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Vasiliki Tsigkou Gerasimos Siasos Evangelos Oikonomou Evanthia Bletsa Manolis Vavuranakis Dimitris Tousoulis 《World Journal of Virology》2022,11(4):216
Coronavirus disease 2019 (COVID-19) is associated with poor cardiovascular outcomes in patients with heart failure (HF) of all categories of ejection fraction (EF), but mainly in patients with HF with reduced EF. Moreover, cardiac transplant patients exhibit worse cardiovascular prognosis, high mortality, and more admissions to the intensive care unit. In general, COVID-19 seems to de-teriorate the clinical status of HF and favors the development of acute respiratory distress syndrome and multiorgan failure, especially in the presence of cardiovascular comorbidities such as diabetes mellitus, kidney dysfunction, and older age. COVID-19 may induce new-onset HF with complex mechanisms that involve myocardial injury. Indeed, myocardial injury comprises a large category of detrimental effects for the myocardium, such as myocardial infarction type 1 or type 2, Takotsubo cardiomyopathy, microvascular dysfunction and myocarditis, which are not easily distinguished by HF. The pathophysiologic mechanisms mainly involve direct myocardial damage by severe acute respiratory syndrome coronavirus 2, cytokine storm, hypercoagulation, inflammation, and endothelial dysfunction. The proper management of patients with COVID-19 involves careful patient evaluation and ongoing monitoring for complications such as HF. 相似文献
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Ioannis Papaconstantinou Evanthia Zampeli Dionysios Dellaportas Charalambos Giannopoulos Maria Sotiropoulou George Polymeneas Giorgos Bamias Spyros Michopoulos 《Clinical journal of gastroenterology》2014,7(2):132-135
Pouchitis occurs in up to one half of patients after restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA). Cytomegalovirus (CMV) and Clostridium difficile are among the commonest secondary identifiable etiologies. A 17-year-old male with ulcerative colitis underwent IPAA due to refractory disease. Nine months later he experienced bloody diarrhea and fever. Laboratory testing and endoscopy confirmed pouch inflammation. Testing for C. difficile toxins A and B was positive. Histology revealed affluent inclusion bodies and immunohistochemistry detected reactivity against CMV protein. Treatment with metronidazole and vancomycin offered partial improvement, whereas the addition of gancyclovir led to a successful recovery. One month after completion of treatment symptoms recurred. Repeat testing precluded an identifiable infectious cause and the diagnosis of idiopathic chronic pouchitis was established. The patient is currently on maintenance treatment with the probiotic compound VSL#3. 相似文献
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Few AP Nanou E Watari H Sullivan JM Scheuer T Catterall WA 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(7):E452-E460
We have identified an asynchronously activated Ca(2+) current through voltage-gated Ca(2+) (Ca(V))-2.1 and Ca(V)2.2 channels, which conduct P/Q- and N-type Ca(2+) currents that initiate neurotransmitter release. In nonneuronal cells expressing Ca(V)2.1 or Ca(V)2.2 channels and in hippocampal neurons, prolonged Ca(2+) entry activates a Ca(2+) current, I(Async), which is observed on repolarization and decays slowly with a half-time of 150-300 ms. I(Async) is not observed after L-type Ca(2+) currents of similar size conducted by Ca(V)1.2 channels. I(Async) is Ca(2+)-selective, and it is unaffected by changes in Na(+), K(+), Cl(-), or H(+) or by inhibitors of a broad range of ion channels. During trains of repetitive depolarizations, I(Async) increases in a pulse-wise manner, providing Ca(2+) entry that persists between depolarizations. In single-cultured hippocampal neurons, trains of depolarizations evoke excitatory postsynaptic currents that show facilitation followed by depression accompanied by asynchronous postsynaptic currents that increase steadily during the train in parallel with I(Async). I(Async) is much larger for slowly inactivating Ca(V)2.1 channels containing β(2a)-subunits than for rapidly inactivating channels containing β(1b)-subunits. I(Async) requires global rises in intracellular Ca(2+), because it is blocked when Ca(2+) is chelated by 10 mM EGTA in the patch pipette. Neither mutations that prevent Ca(2+) binding to calmodulin nor mutations that prevent calmodulin regulation of Ca(V)2.1 block I(Async). The rise of I(Async) during trains of stimuli, its decay after repolarization, its dependence on global increases of Ca(2+), and its enhancement by β(2a)-subunits all resemble asynchronous release, suggesting that I(Async) is a Ca(2+) source for asynchronous neurotransmission. 相似文献
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Bamias G Kaltsa G Siakavellas SI Gizis M Margantinis G Zampeli E Vafiadis-Zoumboulis I Michopoulos S Daikos GL Ladas SD 《Digestive and liver disease》2012,44(1):30-36
Background
TNF-like cytokine 1A provides co-stimulatory signals to activated lymphocytes through binding to death-domain receptor-3. Decoy receptor-3 inhibits death-domain receptor-3 signalling, rendering immunocytes resistant to apoptosis. These functions may be important for the pathogenesis of Crohn's disease.Aims
To study the mucosal and systemic expression of Decoy receptor-3 and TNF-like cytokine 1A in Crohn's disease, in relation to disease activity, localization, and response to treatment.Methods
Soluble Decoy receptor-3 and TNF-like cytokine 1A were measured by ELISA in active or quiescent Crohn's disease. Relative mRNA expression in non-affected and inflamed intestinal mucosa was determined by real-time RT-PCR.Results
We found significant upregulation of Decoy receptor-3 and its ligands TNF-like cytokine 1A and FasL in inflamed intestinal mucosa of Crohn's disease patients. During active disease, Decoy receptor-3 and TNF-like cytokine 1A were detected in the serum in the majority of patients. Intestinal inflammation was strongly associated with these elevations as they were absent during remission and significantly reduced with anti-inflammatory treatment. Regional diversity was observed as Decoy receptor-3 was upregulated in colonic and ileal sites, whereas TNF-like cytokine 1A was preferentially induced in the large bowel mucosa and systemic circulation of patients with colonic involvement.Conclusions
TNF-like cytokine 1A and Decoy receptor-3 are upregulated during active Crohn's disease and may participate in disease pathogenesis and offer novel therapeutic opportunities. 相似文献8.
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Health visitors' perceptions on their role to assess and manage postpartum depression cases in the community
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Foiniki Alexandrou Evanthia Sakellari Michael Kourakos Despina Sapountzi‐Krepia 《Health & social care in the community》2018,26(6):995-1000
The present study gives an insight into the health visitors' perceptions on their role in assessing, managing, and supporting mothers with postpartum depression (PPD). The study took place in Cyprus among health visitors of a community Maternity and Child Welfare Clinic using qualitative approach. Data were collected through individual semistructured interviews. The findings showed that although health visitors are able to identify PPD cases, they stress the importance of protocols and evidence‐based care as well as preventive interventions, and they also point out the importance of home visits. Finally, they support the need for education. It is concluded that health visitors can play an important role in women's health and their intervention on the prevention of PPD in the community especially through home visits is very important. 相似文献
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Kamberoglou DK Zambeli EP Triantafyllopoulos PA Margetis NG Gavalakis NK Tzias VD 《Digestive diseases and sciences》2003,48(12):2242-2246
There is a subgroup of patients with achalasia in which manometry shows elevated intraesophageal pressure, expressed by elevation of esophageal baseline relative to gastric pressure. The aim of this study was to determine the prevalence of elevated intraesophageal pressure in patients with achalasia and its relationship to clinical, radiographic, endoscopic, and other manometric findings. Manometric studies of 62 patients with achalasia were analyzed and elevated intraesophageal pressure was considered any positive elevation of esophageal baseline relative to gastric pressure. Multiple regression analysis was used to determine independent risk factors associated with elevated intraesophageal pressure. Elevated intraesophageal pressure was found in 32 patients (51.6%). Lower esophageal sphincter pressure was the only independent variable associated with elevated intraesophageal pressure (P = 0.0167). Mean lower esophageal sphincter pressure was significantly higher in patients with elevated compared to those with normal intraesophageal pressure (34 +/- 1.96 vs 26.5 +/- 1.73 mm Hg; P = 0.006). In addition, lower esophageal sphincter pressure had a positive correlation with intraesophageal pressure (r = 0.49, P < 0.001). Conversely, no correlation was found between elevated intraesophageal pressure and various symptoms, disease duration, radiologic dilation, a finding of retained fluid during endoscopy, and esophageal length. We conclude that elevated intraesophageal pressure is a common manometric finding in patients with achalasia, with a prevalence of 51.6%, and is associated with significantly higher lower esophageal sphincter pressure. 相似文献