We analyse Kepler observations of the high-amplitude delta Scuti (HADS) star V2367Cyg (KIC9408694). The variations are dominated by a mode with frequency f1= 5.6611d-1. Two other independent modes ...with f2= 7.1490d-1 and f3= 7.7756d-1 have amplitudes an order of magnitude smaller than f1. Nearly all the light variation is due to these three modes and their combination frequencies, but several hundred other frequencies of very low amplitude are also present. The amplitudes of the principal modes may vary slightly with time. The star has twice the projected rotational velocity of any other HADS star, which makes it unusual. We find a correlation between the phases of the combination frequencies and their pulsation frequencies, which is not understood. Since modes of highest amplitude in HADS stars are normally radial modes, we assumed that this would also be true in this star. However, attempts to model the observed frequencies as radial modes without mode interaction were not successful. For a star with such a relatively high rotational velocity, it is important to consider the effect of mode interaction. Indeed, when this was done, we were able to obtain a model in which a good match with f1 and f2 is obtained, with f1 being the fundamental radial mode.
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BFBNIB, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK
Stable gastric pentadecapeptide BPC 157 was suggested to link inflammatory bowel disease and multiple sclerosis, and thereby, shown to equally counteract the models of both of those diseases. For ...colitis, cysteamine (400 mg/kg intrarectally (1 ml/rat)) and colon-colon anastomosis (sacrifice at day 3, 5, 7, and 14) were used. BPC 157 (10 μg/kg, 10 ng/kg) was applied either intraperitoneally once time daily (first application immediately after surgery, last at 24 hours before sacrifice) or per-orally in drinking water (0.16 μg/ml/12 ml/day till the sacrifice) while controls simultaneously received an equivolume of saline (5 ml/kg) intraperitoneally or drinking water only (12 ml/day). A multiple sclerosis suited toxic rat model, cuprizone (compared with standard, a several times higher regimen, 2.5% of diet regimen + 1 g/kg intragastrically/day) was combined with BPC 157 (in drinking water 0.16 μg or 0.16 ng/ml/12 ml/day/rat + 10 μg or 10 ng/kg intragastrically/day) till the sacrifice at day 4. In general, the controls could not heal cysteamine colitis and colon-colon anastomosis. BPC 157 induced an efficient healing of both at the same time. Likewise, cuprizone-controls clearly exhibited an exaggerated and accelerated damaging process; nerve damage appeared in various brain areas, with most prominent damage in corpus callosum, laterodorsal thalamus, nucleus reunions, anterior horn motor neurons. BPC 157-cuprizone rats had consistently less nerve damage in all damaged areas, especially in those areas that otherwise were most affected. Consistently, BPC 157 counteracted cerebellar ataxia and impaired forelimb function. Thereby, this experimental evidence advocates BPC 157 in both inflammatory bowel disease and multiple sclerosis therapy.
With therapy with BPC 157 (known to inhibit nonselective NSAIDs-gastrointestinal, liver and brain-toxicity) and L-arginine, we attempted to discriminate the full complexity of lesions ...(gastrointestinal, liver, brain) after high dose celecoxib administration; the aggravation (that mimics attempt to relieve pain (i.e., selective NSAID as COX-2 inhibition) and NOS-blockade (L-NAME)) along with a possible therapy success and the mechanism(s) behind all of these phenomena. In Wistar rats celecoxib (1 g/kg bw ip) induced severe gastric lesions and less severe duodenal and intestinal lesions with gradual increase from 24 h to 48 h after administration, and sustained level of liver and brain lesions. All these lesions were aggravated by L-NAME (5 mg/ kg bw ip immediately after celecoxib). As the needed proof of NO-system specific involvement, (L-arginine; L-NAME + L-arginine), L-arginine (100 mg/kg bw ip immediately after celecoxib) exhibited a limited beneficial effect (i.e., only after 48 h) while L-NAME + L arginine protocol turned down L-NAME-aggravation to the control-celecoxib presentation at both 24 h and 48 h period. Thus, L-arginine was consistently more active given together with L-NAME (thus, more against L-NAME, less against celecoxib, less against COX-2 inhibition, COX-2-inhibition remains mostly preserved). Contrary, given alone BPC 157 (10 microg, 10 ng/kg bw ip immediately after celecoxib) completely turned down lesions induced by celecoxib, both at 24 h and 48 h. Likewise, the same beneficial effect was consistently evident in all increasingly negative circumstances of celecoxib and L-NAME application and in all BPC 157-groups (L-arginine + BPC 157; L-NAME + BPC 157; L-NAME + L-arginine + BPC 157). Thereby, these findings evidenced that BPC 157 may equally counteract both COX-2 inhibition (celecoxib-noxious effect on all lesions counteracted) and additional NOS-blockade (celecoxib + L-NAME-noxious effect also equally counteracted).
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
There are well-known gender differences in mortality of patients with ST-elevation myocardial infarction (STEMI). Our purpose was to assess factors of hospital mortality separately for men and women ...with STEMI, which are less well known.
In 2018-2019, 485 men and 214 women with STEMI underwent treatment with primary percutaneous coronary intervention (PCI). We retrospectively compared baseline characteristics, treatments and hospital complications between men and women, as well as between nonsurviving and surviving men and women with STEMI.
Primary PCI was performed in 94% of men and 91.1% of women with STEMI, respectively. The in-hospital mortality was significantly higher in women than in men (14% vs 8%, p=0.019). Hospital mortality in both genders was associated significantly to older age, heart failure, prior resuscitation, acute kidney injury, to less likely performed and less successful primary PCI and additionally in men to hospital infection and in women to bleeding. In men and women ≥65 years, mortality was similar (13.3% vs 17.8%, p = 0.293).
Factors of hospital mortality were similar in men and women with STEMI, except bleeding was more likely observed in nonsurviving women and infection in nonsurviving men.
Background: Air pollution with increased concentrations of fine (< 2.5 μm) particulate matter (PM2.5) increases the risk of cardiovascular morbidity and mortality. Even short-term increase of PM2.5 ...may help trigger ST-elevation myocardial infarction (STEMI) and heart failure (HF) in susceptible individuals, even in areas with good air quality. Purpose: To evaluate the role of PM2.5 levels ≥ 20 μg/m3 in admission acute HF in STEMI patients. Materials and Methods: In 290 STEMI patients with the leading reperfusion strategy primary percutaneous coronary intervention (PPCI), we retrospectively studied independent predictors of admission acute HF and included admission demographic and clinical data as well as ambient PM2.5 levels ≥ 20 μg/m3. We defined admission acute HF in STEMI patients as classes II–IV by Killip Kimball classification. Results: Acute admission HF was observed in 34.5% of STEMI patients. PPCI was performed in 87.1% of acute admission HF patients and in 94.7% non-HF patients (p= 0.037). Significant independent predictors of acute admission HF were prior diabetes (OR 2.440, 95% CI 1.100 to 5.400, p=0.028), admission LBBB (OR 10.190, 95% CI 1.160 to 89.360, p=0.036), prior resuscitation (OR 2.530, 95% CI 1.010 to 6.340, p=0.048), admission troponin I≥ 5μg/l (OR 3.390, 95% CI 1.740 to 6.620, p< 0.001), admission eGFR levels (0.61, 95% CI 0.52 to 0.72, p < 0.001), and levels of PM2.5 ≥ 20 μg/m3 (OR 2.140, 95% CI 1.005 to 4.560, p=0.049) one day before admission. Conclusion: Temporary short-term increase in PM2.5 levels (≥ 20 μg/m3) one day prior to admission in an area with mainly good air quality was among significant independent predictors of acute admission HF in STEMI patients.
Climate change is increasing the intensity and frequency of extreme heat events. Ecological responses to extreme heat will depend on vegetation physiology and thermal tolerance. Here we report that ...Larix sibirica, a foundation species across boreal Eurasia, is vulnerable to extreme heat at its southern range margin due to its low thermal tolerance (Tcrit of photosynthesis: ~ 37–48 °C). Projections from CMIP6 Earth System Models (ESMs) suggest that leaf temperatures might exceed the 25th percentile of Larix sibirica’s Tcrit by two to three days per year within the next two to three decades (by 2050) under high emission scenarios (SSP3-7.0 and SSP5-8.5). This degree of warming will threaten the biome’s continued ability to assimilate and sequester carbon. This work highlights that under high emission trajectories we may approach an abrupt ecological tipping point in southern boreal Eurasian forests substantially sooner than ESM estimates that do not consider plant thermal tolerance traits.
While very rarely reported, duodenocutanenous fistula research might alter the duodenal ulcer disease background and therapy. Our research focused on rat duodenocutaneous fistulas, therapy, stable ...gastric pentadecapeptide BPC 157, an anti-ulcer peptide that healed other fistulas, nitric oxide synthase-substrate L-arginine, and nitric oxide synthase-inhibitor L-nitro-arginine methyl ester (L-NAME). The hypothesis was, duodenal ulcer-healing, like the skin ulcer, using the successful BPC 157, with nitric oxide-system involvement, the "wound healing-therapy", to heal the duodenal ulcer, the fistula-model that recently highlighted gastric and skin ulcer healing. Pressure in the lower esophageal and pyloric sphincters was simultaneously assessed. Duodenocutaneous fistula-rats received BPC 157 (10 μg/kg or 10 ng/kg, intraperitoneally or perorally (in drinking water)), L-NAME (5 mg/kg intraperitoneally), L-arginine (100 mg/kg intraperitoneally) alone and/or together, throughout 21 days. Duodenocutaneous fistula-rats maintained persistent defects, continuous fistula leakage, sphincter failure, mortality rate at 40% until the 4(th) day, all fully counteracted in all BPC 157-rats. The BPC 157-rats experienced rapidly improved complete presentation (maximal volume instilled already at 7(th) day). L-NAME further aggravated the duodenocutaneous fistula-course (mortality at 70% until the 4(th) day); L-arginine was beneficial (no mortality; however, maximal volume instilled not before 21(st) day). L-NAME-worsening was counteracted to the control level with the L-arginine effect, and vice versa, while BPC 157 annulled the L-NAME effects (L-NAME + L-arginine; L-NAME + BPC 157; L-NAME + L-arginine + BPC 157 brought below the level of the control). It is likely that duodenocutaneous fistulas, duodenal/skin defect simultaneous healing, reinstated sphincter function, are a new nitric oxide-system related phenomenon. In conclusion, resolving the duodenocutanenous fistulashealing, nitric oxide-system involvement, should illustrate further wound healing therapy to heal duodenal ulcers.
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