Health promoting behaviour of medical versus non-medical students during COVID-19 pandemic: results from the COLA cross-sectional study.

To investigate the COVID-19 pandemic related alteration of health promoting behaviour during lockdown among medical students compared to other students.In this cross-sectional study, we enrolled 1940 Bavarian students. Participants were asked to complete an online questionnaire 3 weeks after lockdown implementation, evaluating their lifestyle behaviour focusing on self-reported and objectively assessed physical activity.1154 medical (59.5%) and 786 non-medical (40.5%) students were included (median age 22.0 [IQR, 20.0-25.0], 71.5% female). Physical activity decreased in both groups after lockdown implementation. During lockdown, medical students reported higher physical activity levels compared to non-medical students. This was corroborated by daily step count data assessed by wearables (median steps per day [IQR], 6979 [5218-9348] versus 6581 [4497-8491], p = 0.02). Smoking behaviour during lockdown did not differ between medical and non-medical students (increased in 11.8% vs 13.6%, decreased in 31.9% versus 36.9%).During the COVID-19 pandemic, alteration of lifestyle behaviour among medical students was significantly different compared to non-medical students. This result suggests that medical students are more concerned about health promoting behaviour even in crisis situations.

Molecular imaging of cardiac CXCR4 expression in a mouse model of acute myocardial infarction using a novel 68Ga-mCXCL12 PET tracer.

BACKGROUND: The chemokine receptor CXCR4 and its ligand CXCL12 have been shown to be a possible imaging and therapeutic target after myocardial infarction (MI). The murine-based and mouse-specific 68Ga-mCXCL12 PET tracer could be suitable for serial in vivo quantification of cardiac CXCR4 expression in a murine model of MI. METHODS AND RESULTS: At days 1-6 after MI, mice were intravenously injected with 68Ga-mCXCL12. Autoradiography was performed and the infarct-to-remote ratio (I/R) was determined. In vivo PET imaging with 68Ga-mCXCL12 was conducted on days 1-6 after MI and the percentage of the injected dose (%ID/g) of the tracer uptake in the infarct area was calculated. 18F-FDG-PET was performed for anatomical landmarking. Ex vivo autoradiography identified CXCR4 upregulation in the infarct region with an increasing I/R after 12 hours (1.4 ± 0.3), showing a significant increase until day 2 (4.5 ± 0.6), followed by a plateau phase (day 4) and decrease after 10 days (1.3 ± 1.0). In vivo PET imaging identified similar CXCR4 upregulation in the infarct region which peaked around day 3 post MI (9.7 ± 5.0 %ID/g) and then subsequently decreased by day 6 (2.8 ± 1.0 %ID/g). CONCLUSION: Noninvasive molecular imaging of cardiac CXCR4 expression using a novel, murine-based, and specific 68Ga-mCXCL12 tracer is feasible both ex vivo and in vivo.

Altered nutrition behavior during COVID-19 pandemic lockdown in young adults.

PURPOSE: The COVID-19 pandemic and the implemented lockdown strongly impact on everyone's daily life. Stressful situations are known to alter eating habits and increase the risk for obesity. In our study, we aimed to investigate the effect of the lockdown measures on nutrition behavior among young adults. METHODS: In this cross-sectional study, we enrolled 1964 voluntary participants from Bavarian universities. All participants were asked to complete an online questionnaire, semi-quantitatively evaluating the amount and type of food before and during pandemic lockdown. Study subjects were inquired to give information about acquisition and food procurement. The primary outcome was the change in food amount, secondary outcomes included alterations of food composition and procurement. RESULTS: Our study cohort (mean age 23.3 ± 4.0 years, 28.5% male) had a mean body mass index of 22.1 ± 4.5 kg/m2. The overall food amount increased in 31.2% of participants (n = 610) during lockdown and decreased in 16.8% (n = 328). A multinominal regression model revealed that an increased food intake was less likely in male participants (OR, 0.7 [CI 0.6-0.9]) and more likely with increasing BMI (OR, 1.4 [CI 1.3-2.0]), increased sports activity (OR, 1.3 [CI 1.2-1.8]), augmented mental stress (OR 1.4 [1.1-1.7]), and an alteration of alcohol consumption (reduced alcohol amount, OR, 1.4 [CI 1.1-1.7], increased alcohol, OR, 1.9 [CI 1.4-2.5]). Increase in food intake was mainly triggered by consumption of bread (increased in 46.8%, n = 284) and confectionary (increased in 64.4%, n = 389). CONCLUSION: The COVID-19 pandemic lockdown significantly affected eating habits in young adults. Further investigation to evaluate long-term effects on weight change and comorbidities are warranted.

Altered alcohol consumption during COVID-19 pandemic lockdown.

BACKGROUND: Since the onset of the COVID-19 pandemic in December 2019, many countries around the world have imposed lockdown measures in order to reduce virus spread. Social isolation is known to have a significant psychological impact, potentially triggering alcohol misuse in adults. In our study, we aimed to investigate the effect of COVID-19 lockdown measures on alcohol consumption in adults in Bavaria. METHODS: In this cross-sectional study, we enrolled 2067 participants, with 1961 young adults (mean age 23.3 ± 4.1) and 106 mature adults (mean age 66.7 ± 9.7). Participants were asked to complete a standardized questionnaire, semi-quantitatively evaluating the alcohol drinking behaviour before and during the pandemic lockdown. RESULTS: After implementation of lockdown, the alteration of alcohol consumption was significantly different between young and mature adults (p <  0.001). Among young adults, 42% reported unchanged drinking behaviour compared to 76% in the mature adult group; 44% of young adults reported to drink less compared to only 7% of mature adults. An increase in alcohol consumption was only reported by 14% of young adults and 17% of mature adults. Interestingly, in the entire cohort, the change of alcohol intake was most pronounced among moderate drinkers (> 0 to < 5 drinks/week) in both age groups (p <  0.001). Ordinal logistic regression revealed female sex, low BMI and younger age to be associated with a decrease in number of self-reported drinks/week. CONCLUSION: The COVID-19 pandemic lockdown significantly affected alcohol drinking behaviour. Further studies exploring long-term effects on potential alcohol misuse and the relevance on public health are warranted. TRIAL REGISTRATION: The study was retrospectively registered at ClinicalTrials.gov ( NCT04361877 ) on April 24, 2020.

Feasibility and accuracy of SPECT myocardial perfusion imaging in end-stage lung disease.

BACKGROUND: Coronary artery disease (CAD) is associated with increased mortality in patients with chronic lung disease. However, non-invasive diagnostic of CAD is difficult, especially in patients with more advanced disease. Therefore, we aimed to assess the feasibility and accuracy of SPECT-myocardial perfusion imaging (MPI) stress testing with regadenoson in patients with end-stage lung disease (ELD) undergoing assessment of stable CAD. METHODS: Between January 2012 and May 2018, 102 patients with ELD, who were referred to our institution for lung transplant evaluation, were assessed retrospectively. All patients underwent both stress SPECT-MPI as well as coronary angiography. RESULTS: The mean age in our population was 57±6 years. All patients had severe pulmonary function impairment. During stress SPECT-MPI 14 patients (14%) reported regadenoson-related symptoms, but only 2 patients (2%) required medical treatment. Coronary angiography revealed obstructive CAD in 20 patients (20%). Among those, 5 patients had abnormal SPECT-MPI and PCI was performed in 3 patients accordingly. In 14 patients with obstructive CAD, revascularization was deferred based on normal SPECT-MPI findings. CONCLUSIONS: SPECT-MPI using regadenoson is well tolerated in patients with ELD and can help to make decisions about coronary revascularization before lung transplant.

Microfluidic Single-Cell Analysis of Transplanted Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes After Acute Myocardial Infarction.

BACKGROUND: Human induced pluripotent stem cells (iPSCs) are attractive candidates for therapeutic use, with the potential to replace deficient cells and to improve functional recovery in injury or disease settings. Here, we test the hypothesis that human iPSC-derived cardiomyocytes (iPSC-CMs) can secrete cytokines as a molecular basis to attenuate adverse cardiac remodeling after myocardial infarction. METHODS AND RESULTS: Human iPSCs were generated from skin fibroblasts and differentiated in vitro with a small molecule-based protocol. Troponin(+) iPSC-CMs were confirmed by immunohistochemistry, quantitative polymerase chain reaction, fluorescence-activated cell sorting, and electrophysiological measurements. Afterward, 2×10(6) iPSC-CMs derived from a cell line transduced with a vector expressing firefly luciferase and green fluorescent protein were transplanted into adult NOD/SCID mice with acute left anterior descending artery ligation. Control animals received PBS injection. Bioluminescence imaging showed limited engraftment on transplantation into ischemic myocardium. However, magnetic resonance imaging of animals transplanted with iPSC-CMs showed significant functional improvement and attenuated cardiac remodeling compared with PBS-treated control animals. To understand the underlying molecular mechanism, microfluidic single-cell profiling of harvested iPSC-CMs, laser capture microdissection of host myocardium, and in vitro ischemia stimulation were used to demonstrate that the iPSC-CMs could release significant levels of proangiogenic and antiapoptotic factors in the ischemic microenvironment. CONCLUSIONS: Transplantation of human iPSC-CMs into an acute mouse myocardial infarction model can improve left ventricular function and attenuate cardiac remodeling. Because of limited engraftment, most of the effects are possibly explained by paracrine activity of these cells.

Attenuation of cardiac hypertrophy by G-CSF is associated with enhanced migration of bone marrow-derived cells.

Granulocyte-colony stimulating factor (G-CSF) has been shown to promote mobilization of bone marrow-derived stem cells (BMCs) into the bloodstream associated with improved survival and cardiac function after myocardial infarction. Therefore, the aim of the present study was to investigate whether G-CSF is able to attenuate cardiac remodelling in a mouse model of pressure-induced LV hypertrophy focusing on mobilization and migration of BMCs. LV hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6J mice. Four weeks after TAC procedure. Mice were treated with G-CSF (100 µg/kg/day; Amgen Biologicals) for 2 weeks. The number of migrated BMCs in the heart was analysed by flow cytometry. mRNA expression and protein level of different growth factors in the myocardium were investigated by RT-PCR and ELISA. Functional analyses assessed by echocardiography and immunohistochemical analysis were performed 8 weeks after TAC procedure. G-CSF-treated animals revealed enhanced homing of VLA-4(+) and c-kit(+) BMCs associated with increased mRNA expression and protein level of the corresponding homing factors Vascular cell adhesion protein 1 and Stem cell factor in the hypertrophic myocardium. Functionally, G-CSF significantly preserved LV function after TAC procedure, which was associated with a significantly reduced area of fibrosis compared to control animals. Furthermore, G-CSF-treated animals revealed a significant improvement of survival after TAC procedure. In summary, G-CSF treatment preserves cardiac function and is able to diminish cardiac fibrosis after induction of LV hypertrophy associated with increased homing of VLA-4(+) and c-kit(+) BMCs and enhanced expression of their respective homing factors VCAM-1 and SCF.

Increased numbers of bone marrow-derived cells in parathyroid adenoma.

BACKGROUND: In primary hyperparathyroidism (PHPT), the increased levels of parathyroid hormone (PTH) result in mobilisation of bone-marrow-derived cells (BMCs) into peripheral blood. However, the fate of these cells is still unknown. MATERIALS AND METHODS: In this study, we sought to investigate cells with typical surface markers of BMCs within parathyroid adenomas (PA) of patients with primary hyperparathyroidism. We therefore investigated PA and normal parathyroid glands (NPG) of 15 patients with PHPT by immunohistochemistry and PCR. RESULTS: mRNA levels for CD31, CD34 and CD45 were significantly increased in PA compared to NPG. Immunohistochemical staining for CD31 and CD34 revealed a significantly higher vessel density in PA. Furthermore, scattered single cells expressing CD31, CD34 or CD45 were significantly augmented compared to normal parathyroid glands and directly correlated with vessel density. mRNA levels of SDF-1 was increased whereas its major inhibitor dipeptidylpeptidase IV (DPP IV) is decreased in PA, suggesting that the SDF-1 axis plays a role in the migration of BMCs into PA. CONCLUSION: These data indicate a possible role of BMCs in the pathophysiology of PA of patients with PHPT.

Costimulation-adhesion blockade is superior to cyclosporine A and prednisone immunosuppressive therapy for preventing rejection of differentiated human embryonic stem cells following transplantation.

RATIONALE: Human embryonic stem cell (hESC) derivatives are attractive candidates for therapeutic use. The engraftment and survival of hESC derivatives as xenografts or allografts require effective immunosuppression to prevent immune cell infiltration and graft destruction. OBJECTIVE: To test the hypothesis that a short-course, dual-agent regimen of two costimulation-adhesion blockade agents can induce better engraftment of hESC derivatives compared to current immunosuppressive agents. METHODS AND RESULTS: We transduced hESCs with a double fusion reporter gene construct expressing firefly luciferase (Fluc) and enhanced green fluorescent protein, and differentiated these cells to endothelial cells (hESC-ECs). Reporter gene expression enabled longitudinal assessment of cell engraftment by bioluminescence imaging. Costimulation-adhesion therapy resulted in superior hESC-EC and mouse EC engraftment compared to cyclosporine therapy in a hind limb model. Costimulation-adhesion therapy also promoted robust hESC-EC and hESC-derived cardiomyocyte survival in an ischemic myocardial injury model. Improved hESC-EC engraftment had a cardioprotective effect after myocardial injury, as assessed by magnetic resonance imaging. Mechanistically, costimulation-adhesion therapy is associated with systemic and intragraft upregulation of T-cell immunoglobulin and mucin domain 3 (TIM3) and a reduced proinflammatory cytokine profile. CONCLUSIONS: Costimulation-adhesion therapy is a superior alternative to current clinical immunosuppressive strategies for preventing the post-transplant rejection of hESC derivatives. By extending the window for cellular engraftment, costimulation-adhesion therapy enhances functional preservation following ischemic injury. This regimen may function through a TIM3-dependent mechanism.

Microfluidic single-cell analysis shows that porcine induced pluripotent stem cell-derived endothelial cells improve myocardial function by paracrine activation.

RATIONALE: Induced pluripotent stem cells (iPSCs) hold great promise for the development of patient-specific therapies for cardiovascular disease. However, clinical translation will require preclinical optimization and validation of large-animal iPSC models. OBJECTIVE: To successfully derive endothelial cells from porcine iPSCs and demonstrate their potential utility for the treatment of myocardial ischemia. METHODS AND RESULTS: Porcine adipose stromal cells were reprogrammed to generate porcine iPSCs (piPSCs). Immunohistochemistry, quantitative PCR, microarray hybridization, and angiogenic assays confirmed that piPSC-derived endothelial cells (piPSC-ECs) shared similar morphological and functional properties as endothelial cells isolated from the autologous pig aorta. To demonstrate their therapeutic potential, piPSC-ECs were transplanted into mice with myocardial infarction. Compared with control, animals transplanted with piPSC-ECs showed significant functional improvement measured by echocardiography (fractional shortening at week 4: 27.2±1.3% versus 22.3±1.1%; P<0.001) and MRI (ejection fraction at week 4: 45.8±1.3% versus 42.3±0.9%; P<0.05). Quantitative protein assays and microfluidic single-cell PCR profiling showed that piPSC-ECs released proangiogenic and antiapoptotic factors in the ischemic microenvironment, which promoted neovascularization and cardiomyocyte survival, respectively. Release of paracrine factors varied significantly among subpopulations of transplanted cells, suggesting that transplantation of specific cell populations may result in greater functional recovery. CONCLUSIONS: In summary, this is the first study to successfully differentiate piPSCs-ECs from piPSCs and demonstrate that transplantation of piPSC-ECs improved cardiac function after myocardial infarction via paracrine activation. Further development of these large animal iPSC models will yield significant insights into their therapeutic potential and accelerate the clinical translation of autologous iPSC-based therapy.

In vivo functional and transcriptional profiling of bone marrow stem cells after transplantation into ischemic myocardium.

OBJECTIVE: Clinical trials of bone marrow-derived stem cell therapy for the heart have yielded variable results. The basic mechanism(s) that underlies their potential efficacy remains unknown. In the present study, we evaluated the survival kinetics, transcriptional response, and functional outcome of intramyocardial bone marrow mononuclear cell (BMMC) transplantation for cardiac repair in a murine myocardial infarction model. METHODS AND RESULTS: We used bioluminescence imaging and high-throughput transcriptional profiling to evaluate the in vivo survival kinetics and gene expression changes of transplanted BMMCs after their engraftment into ischemic myocardium. Our results demonstrate short-lived survival of cells following transplant, with less than 1% of cells surviving by 6 weeks posttransplantation. Moreover, transcriptomic analysis of BMMCs revealed nonspecific upregulation of various cell regulatory genes, with a marked downregulation of cell differentiation and maturation pathways. BMMC therapy caused limited improvement of heart function as assessed by echocardiography, invasive hemodynamics, and positron emission tomography. Histological evaluation of cell fate further confirmed findings of the in vivo cell tracking and transcriptomic analysis. CONCLUSIONS: Collectively, these data suggest that BMMC therapy, in its present iteration, may be less efficacious than once thought. Additional refinement of existing cell delivery protocols should be considered to induce better therapeutic efficacy.

Migration of bone marrow-derived cells and improved perfusion after treatment with erythropoietin in a murine model of myocardial infarction.

Erythropoietin (EPO) was shown to have protective effects after myocardial infarction (MI) by neovascularization and antiapoptotic mechanisms. Beside direct receptor-dependent mechanisms, mobilization and homing of bone marrow-derived cells (BMCs) may play a pivotal role in this regard. In this study, we intended to track different subpopulations of BMCs and to assess serially myocardial perfusion changes in EPO-treated mice after MI. To allow tracking of BMCs, we used a chimeric mouse model. Therefore, mice (C57BL/6J) were sublethally irradiated, and bone marrow (BM) from green fluorescent protein transgenic mice was transplanted. Ten weeks later coronary artery ligation was performed to induce MI. EPO was injected for 3 days with a total dose of 5000 IU/kg. Subpopulations (CD31, c-kit, CXCR-4 and Sca-1) of EGFP(+) cells were studied in peripheral blood, bone marrow and hearts by flow cytometry. Myocardial perfusion was serially investigated in vivo by pinhole single-photon emission computed tomography (SPECT) at days 6 and 30 after MI. EPO-treated animals revealed an enhanced mobilization of BMCs into peripheral blood. The numbers of these cells in BM remained unchanged. Homing of all BMCs subpopulations to the ischaemic myocardium was significantly increased in EPO-treated mice. Among the investigated subpopulations, EPO predominantly affected migration of CXCR-4(+) (4.3-fold increase). Repetitively SPECT analyses revealed a reduction of perfusion defects after EPO treatment over time. Our study shows that EPO treatment after MI enhances the migration capacity of BMCs into ischaemic tissue, which may attribute to an improved perfusion and reduced size of infarction, respectively.

Cardiac arrest associated with sildenafil ingestion in a patient with an abnormal origin of the left coronary artery: case report.

BACKGROUND: Left coronary artery arising from the right sinus of Valsalva is an uncommon congenital coronary anomaly that seems to be associated with sudden death in young patients. CASE PRESENTATION: We report a case of cardiac arrest in a 59-year-old patient after sexual intercourse and Sildenafil ingestion. A coronary arteriography and an angiographic computed tomography scan subsequently revealed a LCA origin from the right aortic sinus along with an intramural course of the left main stem. In addition a distal stenosis of the right coronary artery was detected. After successful resuscitation without neurological deficits coronary artery bypass surgery was performed. CONCLUSION: To our knowledge, this is the first report demonstrating sudden cardiac arrest associated with Sildenafil ingestion in a patient with this type of coronary anomaly. The question arises, whether a cardiac screening is necessary before a Sildenafil therapy is initiated.

Outcome of patients treated with extracorporeal life support in cardiogenic shock complicating acute myocardial infarction: 1-year result from the ECLS-Shock study.

BACKGROUND: Treatment with extracorporeal life support (ECLS) in acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) fell short of improving myocardial recovery measured by 30 day ejection fraction in the ECLS-SHOCK trial. However, to date, no data regarding impact of ECLS on long-term outcomes exist. METHODS: In this randomized, controlled, prospective, open-label trial, 42 patients with CS complicating AMI were randomly assigned to ECLS (ECLS group, n = 21) or no ECLS (control group, n = 21). The primary endpoint was left ventricular ejection fraction (LVEF) after 30 days. Secondary endpoints included mortality and neurological outcome after 12 months. Evaluation of neurological outcome used the modified Rankin Scale. RESULTS: The 12-month all-cause mortality was 19% in the ECLS group versus 38% in the control group (p = 0.31). Only one patient (control group) died after the initial 30 days. Three patients underwent elective percutaneous coronary intervention (PCI) during follow-up (one in the control and two in the ECLS group). Favorable neurological outcome (modified Rankin Score ≤ 2) was seen in 61.9% of patients in the ECLS group versus 57.1% in the control group (p = 1). CONCLUSION: This pilot study showed that randomized studies with ECLS in CS patients are feasible and safe. Small numbers of included patients impede meaningful conclusions about mortality and neurological outcome. Our findings of numerical differences in mortality and survival with severe neurological impairment give an urgent call for larger multi-centric randomized trials assessing the endpoint of all-cause mortality but also considering the effects on neurological outcome measures.

Comparison of parathyroid hormone and G-CSF treatment after myocardial infarction on perfusion and stem cell homing.

Mobilization of stem cells by granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI); however, clinical trials failed to be effective. In search for alternative cytokines, parathyroid hormone (PTH) was recently shown to promote cardiac repair by enhanced neovascularization and cell survival. To compare the impact of the two cytokines G-CSF and PTH on myocardial perfusion, mice were noninvasively and repetitively investigated by pinhole single-photon emission computed tomography (SPECT) after MI. Mobilization and homing of bone marrow-derived stem cells (BMCs) was analyzed by fluorescence-activated cell sorter (FACS) analysis. Mice (C57BL/6J) were infarcted by left anterior descending artery ligation. PTH (80 mug/kg) and G-CSF (100 mug/kg) were injected for 5 days. Perfusion defects were determined by (99m)Tc-sestamibi SPECT at days 6 and 30 after MI. The number of BMCs characterized by Lin(-)/Sca-1(+)/c-kit(+) cells in peripheral blood and heart was analyzed by FACS. Both G-CSF and PTH treatment resulted in an augmented mobilization of BMCs in the peripheral blood. Contrary to G-CSF and controls, PTH and the combination showed significant migration of BMCs in ischemic myocardium associated with a significant reduction of perfusion defects from day 6 to day 30. A combination of both cytokines had no additional effects on migration and perfusion. In our preclinical model, SPECT analyses revealed the functional potential of PTH reducing size of infarction together with an enhanced homing of BMCs to the myocardium in contrast to G-CSF. A combination of both cytokines did not improve the functional outcome, suggesting clinical applications of PTH in ischemic heart diseases.

Erythropoietin administration after myocardial infarction in mice attenuates ischemic cardiomyopathy associated with enhanced homing of bone marrow-derived progenitor cells via the CXCR-4/SDF-1 axis.

Mobilization of bone marrow-derived stem cells (BMCs) was shown to have protective effects after myocardial infarction (MI). However, the classical mobilizing agent, granulocyte-colony stimulating factor (G-CSF) relapsed after revealing an impaired homing capacity. In the search for superior cytokines, erythropoietin (EPO) appears to be a promising agent. Therefore, we analyzed in a murine model of surgically induced MI the influence of EPO treatment on survival and functional parameters as well as BMC mobilization, homing, and effect on resident cardiac stem cells (CSCs). Human EPO was injected intraperitoneally after ligation of the left anterior descendens (LAD) for 3 days with a total dose of 5000 IU/kg 6 and 30 days after MI, and pressure volume relationships were investigated in vivo. Cardiac tissues were analyzed by histology. To show the effect on BMCs and CSCs, FACS analyses were performed. Homing factors were analyzed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and ELISA. EPO-treated animals showed a significant improvement of survival post-MI (62 vs. 36%). At days 6 and 30, all hemodynamic parameters associated with attenuated remodeling, enhanced neovascularization, and diminished apoptotic cells in the peri-infarct area were improved. BMC subpopulations (CD31(+), c-kit(+), and Sca-1(+) cells) were mobilized, and homing of Sca-1(+) and CXCR4(+) BMCs toward an SDF-1 gradient into the ischemic myocardium was enhanced. However, there was no beneficial effect on CSCs. We have shown that EPO application after MI shows cardioprotective effects. This may be explained by mobilization of BMCs, which are homing via the CXCR-4/SDF-1 axis. However, EPO has no beneficial effects on resident CSCs. Therefore, new treatment regimes using EPO together with other agents may combine complementary beneficial effects preventing ischemic cardiomyopathy.

[Q-fever - a rare cause for myocarditis]. / Q-Fieber ­ seltene Ursache einer Myokarditis.

PATIENT HISTORY: A 33-year old Romanian chef presented with sudden onset of chest pain and chills as well as a significant elevation of myocardial markers and CRP. EXAMS: Coronary angiography showed no signs of relevant atherosclerosis. A myocarditis was assumed and later diagnosed on cardiac MRI. DIAGNOSTICS: Due to fevers up to 40 °C and occupational history, Q fever was assumed. Serologic findings confirmed the diagnosis. THERAPY AND COURSE OF EVENTS: After the start of antibiotic treatment, temperatures remained normal and the patient could be discharged a few days later. Azithromycin was recommended for several weeks to prevent a chronic infection. At the check-up visit one month later the patient appeared to have no signs of chronic heart failure or persistent infection. CONCLUSIONS: Myocarditis is a rare manifestation of Q fever, which should not be missed. The diagnostic evaluation with antibody titers is easy. The antibiotic therapy is well tolerated and is a causal treatment that helps to prevent long-term damage.

Mental health impairment triggered by the COVID-19 pandemic in a sample population of German students.

Due to the rapid spread of the COVID-19 pandemic, a lockdown including limitation of activity and restrictions of non-essential travel was imposed on March 21, 2020 in the State of Bavaria, Germany. The implementation of activity restrictions not only strongly affects the economy but will possibly also impact the mental and physical health status of the general population. Therefore, the present study aimed to explore psychological effects of the COVID-19 crisis on a sample of Bavarian students.In this cross-sectional study, we enrolled 1943 voluntary subjects from Bavarian universities. All subjects completed an online questionnaire asking for mental health stress, as well as potential factors, influencing the state of mental stress during pandemic lockdown. In our study cohort, 17.3% (n=336) of the students indicated that they experienced less mental stress through COVID-19 pandemic, while 39.6% (n=770) stated that they had an increased psychological burden. The bivariate analysis identified sex and the level of physical activity as potential risk factors for the level of mental stress during the COVID-19 pandemic. Further research is necessary to investigate specific symptoms of mental stress and the overall long-term impact on mental health.