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  • S. Karger AG  (21)
  • Pharmacy  (21)
  • 1
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    Online Resource
    Ebolavirus Vaccines: Progress in the Fight Against Ebola Virus Disease
    S. Karger AG ; 2015
    In:  Cellular Physiology and Biochemistry Vol. 37, No. 5 ( 2015), p. 1641-1658
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 37, No. 5 ( 2015), p. 1641-1658
    Abstract: Ebolaviruses are highly infectious pathogens that cause lethal Ebola virus disease (EVD) in humans and non-human primates (NHPs). Due to their high pathogenicity and transmissibility, as well as the potential to be misused as a bioterrorism agent, ebolaviruses would threaten the health of global populations if not controlled. In this review, we describe the origin and structure of ebolaviruses and the development of vaccines from the beginning of the 1980s, including conventional ebolavirus vaccines, DNA vaccines, Ebola virus-like particles (VLPs), vaccinia virus-based vaccines, Venezuelan equine encephalitis virus (VEEV)-like replicon particles, Kunjin virus-based vaccine, recombinant Zaire Ebolavirus∆VP30, recombinant cytomegalovirus (CMV)-based vaccines, recombinant rabies virus (RABV)-based vaccines, recombinant paramyxovirus-based vaccines, adenovirus-based vaccines and vesicular stomatitis virus (VSV)-based vaccines. No licensed vaccine or specific treatment is currently available to counteract ebolavirus infection, although DNA plasmids and several viral vector approaches have been evaluated as promising vaccine platforms. These vaccine candidates have been confirmed to be successful in protecting NHPs against lethal infection. Moreover, these vaccine candidates were successfully advanced to clinical trials. The present review provides an update of the current research on Ebola vaccines, with the aim of providing an overview on current prospects in the fight against EVD.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000438531
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
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  • 2
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    Post-COVID-19 Epidemic: Allostatic Load among Medical and Nonmedical Workers in China
    S. Karger AG ; 2021
    In:  Psychotherapy and Psychosomatics Vol. 90, No. 2 ( 2021), p. 127-136
    Details
    In: Psychotherapy and Psychosomatics, S. Karger AG, Vol. 90, No. 2 ( 2021), p. 127-136
    Abstract: Background: As the fight against the COVID-19 epidemic continues, medical workers may have allostatic load. Objective: During the reopening of society, medical and nonmedical workers were compared in terms of allostatic load. Methods: An online study was performed; 3,590 Chinese subjects were analyzed. Socio-demographic variables, allostatic load, stress, abnormal illness behavior, global well-being, mental status, and social support were assessed. Results: There was no difference in allostatic load in medical workers compared to nonmedical workers (15.8 vs. 17.8%; p = 0.22). Multivariate conditional logistic regression revealed that anxiety (OR = 1.24; 95% CI 1.18–1.31; p 〈 0.01), depression (OR = 1.23; 95% CI 1.17–1.29; p 〈 0.01), somatization (OR = 1.20; 95% CI 1.14–1.25; p 〈 0.01), hostility (OR = 1.24; 95% CI 1.18–1.30; p 〈 0.01), and abnormal illness behavior (OR = 1.49; 95% CI 1.34–1.66; p 〈 0.01) were positively associated with allostatic load, while objective support (OR = 0.84; 95% CI 0.78–0.89; p 〈 0.01), subjective support (OR = 0.84; 95% CI 0.80–0.88; p 〈 0.01), utilization of support (OR = 0.80; 95% CI 0.72–0.88; p 〈 0.01), social support (OR = 0.90; 95% CI 0.87–0.93; p 〈 0.01), and global well-being (OR = 0.30; 95% CI 0.22–0.41; p 〈 0.01) were negatively associated. Conclusions: In the post-COVID-19 epidemic time, medical and nonmedical workers had similar allostatic load. Psychological distress and abnormal illness behavior were risk factors for it, while social support could relieve it.
    Type of Medium: Online Resource
    ISSN: 0033-3190 , 1423-0348
    URL: Article
    DOI: 10.1159/000511823
    RVK:
    CU 5500
    RVK:
    XA 10000
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2021
    detail.hit.zdb_id: 1472321-9
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  • 3
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    Gamma-Secretase Inhibitors Attenuate Neurotrauma and Neurogenic Acute Lung Injury in Rats by Rescuing the Accumulation of Hypertrophic Microglia
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 44, No. 5 ( 2017), p. 1726-1740
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 44, No. 5 ( 2017), p. 1726-1740
    Abstract: Background/Aims: In response to traumatic brain injury (TBI), activated microglia exhibit changes in their morphology from the resting ramified phenotype toward the activated hypertrophic or amoeboid phenotype. Here, we provide the first description of the mechanism underlying the neuroprotective effects of γ-secretase inhibitors on TBI outcomes in rats. Methods: The neuroprotective effects of γ-secretase inhibitors such as LY411575 or CHF5074 on TBI-induced neurotoxicity were analysed using a neurological motor function evaluation, cerebral contusion assay, immunohistochemical staining for microglia phenotypes, lung injury score and Evans Blue dye extravasation assay of brain and lung oedema. Results: Hypertrophic or amoeboid microglia accumulated in the injured cortex, the blood-brain-barrier was disrupted and neurological deficits and acute lung injury were observed 4 days after TBI in adult rats. However, a subcutaneous injection of LY411575 (5 mg/kg) or CHF5074 (30 mg/kg) immediately after TBI and once daily for 3 consecutive days post-TBI significantly attenutaed the accumulation of hypertrophic microglia in the injured brain, neurological injury, and neurogenic acute lung injury. Conclusion: Gamma-secretase inhibitors attenuated neurotrauma and neurogenic acute lung injury in rats by reducing the accumulation of hypertrophic microglia in the vicinity of the lesion.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000485778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
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  • 4
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    Effects of Sodium-Glucose Cotransporter 2 on Amputation Events: A Systematic Review and Meta-Analysis of Randomized-Controlled Trials
    S. Karger AG ; 2022
    In:  Pharmacology Vol. 107, No. 3-4 ( 2022), p. 123-130
    Details
    In: Pharmacology, S. Karger AG, Vol. 107, No. 3-4 ( 2022), p. 123-130
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are increasingly utilized in the treatment of diabetes mellitus as well as therapeutic extra-glycemic effects. However, there are still concerns over complications such as amputation events, given the results from the Canagliflozin Cardiovascular Assessment Study (CANVAS) trial. Hence, we conducted a systematic review and meta-analysis of randomized-controlled trials to investigate the effect of SGLT2 inhibitors on amputation events. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Four electronic databases (PubMed, Embase, Cochrane, and SCOPUS) were searched on November 21, 2020, for articles published from January 1, 2000, up to November 21, 2020, for studies that examined the effect of SGLT2 inhibitors on amputation events. Random-effect pair-wise meta-analysis for hazard ratios and fixed-effect Peto odds ratio meta-analysis were utilized to summarize the studies. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 A total of 15 randomized-controlled trials were included with a combined cohort of 63,716 patients. We demonstrated that there was no significant difference in amputation events across different types of SGLT2 inhibitors, different baseline populations, and different duration of SGLT2 inhibitor use. 〈 b 〉 〈 i 〉 Discussion/Conclusions: 〈 /i 〉 〈 /b 〉 In this meta-analysis, SGLT2 inhibitors were not associated with a significant difference in amputation events.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000520903
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1483550-2
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  • 5
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    Ubiquitin E3 Ligase A20 Contributes to Maintaining Epithelial Barrier Function
    S. Karger AG ; 2012
    In:  Cellular Physiology and Biochemistry Vol. 30, No. 3 ( 2012), p. 702-710
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 30, No. 3 ( 2012), p. 702-710
    Type of Medium: Online Resource
    ISSN: 1421-9778 , 1015-8987
    URL: Article
    DOI: 10.1159/000341450
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
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  • 6
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    Effect of the Antidepressant Desipramine on Cytosolic Ca〈sup〉2+〈/sup〉 Movement and Proliferation in Human Osteosarcoma Cells
    S. Karger AG ; 2003
    In:  Pharmacology Vol. 69, No. 4 ( 2003), p. 190-196
    Details
    In: Pharmacology, S. Karger AG, Vol. 69, No. 4 ( 2003), p. 190-196
    Abstract: In human osteosarcoma MG63 cells, the effect of desipramine, an antidepressant, on intracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 concentration ([Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 ) was measured by using fura-2. Desipramine ( 〉 10 µmol/l) caused a rapid and sustained rise of [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 in a concentration-dependent manner (EC 〈 sub 〉 50 〈 /sub 〉 = 200 µmol/l). Desipramine-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rise was prevented by 80% by removal of extracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 but was not altered by voltage-gated Ca 〈 sup 〉 2+ 〈 /sup 〉 channel blockers. In Ca 〈 sup 〉 2+ 〈 /sup 〉 -free medium, thapsigargin, an inhibitor of the endoplasmic reticulum (ER) Ca 〈 sup 〉 2+ 〈 /sup 〉 -ATPase, caused a monophasic [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rise, after which the increasing effect of desipramine on [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 was abolished; also, pretreatment with desipramine partly reduced thapsigargin-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 increase. U73122, an inhibitor of phospholipase C, did not affect desipramine-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rise. Overnight incubation with 10 µmol/l desipramine did not alter cell proliferation, but killed 32 and 89% of cells at concentrations of 100 and 200 µmol/l, respectively. These findings suggest that desipramine rapidly increases [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 in osteoblasts by stimulating both extracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 influx and intracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 release, and is cytotoxic at high concentrations.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000073663
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2003
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  • 7
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    Defect in Regulation of Ca〈sup〉2+〈/sup〉 Movement in Platelets from Patients with Systemic Lupus erythematosus
    S. Karger AG ; 2005
    In:  Pharmacology Vol. 73, No. 4 ( 2005), p. 169-174
    Details
    In: Pharmacology, S. Karger AG, Vol. 73, No. 4 ( 2005), p. 169-174
    Abstract: The differences in the intracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 responses to hormones in platelets from systemic lupus erythematosus (SLE) patients compared to normal humans have not been explored. This study examined the Ca 〈 sup 〉 2+ 〈 /sup 〉 signaling and density of platelets in normal, inactive and active SLE patients. The platelet number per µl in inactive and normal groups did not differ, whereas the number in active SLE patients was smaller than the other two groups by 60%. The intracellular free Ca 〈 sup 〉 2+ 〈 /sup 〉 levels ([Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 ) in response to stimulation of four endogenous Ca 〈 sup 〉 2+ 〈 /sup 〉 mobilizing hormones, 100 µ 〈 i 〉 M 〈 /i 〉 arachidonic acid (AA), 10 µ 〈 i 〉 M 〈 /i 〉 ADP, 10 n 〈 i 〉 M 〈 /i 〉 platelet activation factor (PAF) and 1 µ 〈 i 〉 M 〈 /i 〉 thrombin, were investigated using the Ca 〈 sup 〉 2+ 〈 /sup 〉 -sensitive fluorescent dye, fura-2. The AA-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rises in normal and inactive groups were similar. In contrast, the AA-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rises in the active SLE group were significantly smaller than in the normal and inactive groups. The defect in the AA-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rises in active SLE groups appears to be caused by defective Ca 〈 sup 〉 2+ 〈 /sup 〉 influx and Ca 〈 sup 〉 2+ 〈 /sup 〉 releasing pathways because the AA-induced responses were not altered by removal of extracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 , whereas the AA-induced responses in normal and inactive SLE groups were reduced by removal of extracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 , and the AA-induced Ca 〈 sup 〉 2+ 〈 /sup 〉 release was smaller in the active SLE group. PAF, ADP and thrombin all induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 rises in the three groups, but no significant differences were found among the three groups. Together, the results indicate that cell density and Ca 〈 sup 〉 2+ 〈 /sup 〉 signaling in platelets from active SLE patients are altered in response to particular stimulators. In these regards, platelets from inactive SLE patients appear to be similar to those from normal humans.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000082610
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2005
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  • 8
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    Effect of Riluzole on Cytosolic Ca〈sup〉2+〈/sup〉 Increase in Human Osteosarcoma Cells
    S. Karger AG ; 2002
    In:  Pharmacology Vol. 66, No. 3 ( 2002), p. 120-127
    Details
    In: Pharmacology, S. Karger AG, Vol. 66, No. 3 ( 2002), p. 120-127
    Abstract: In human osteosarcoma MG63 cells, the effect of the neuroprotective drug riluzole on the intracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 concentration ([Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 ) was measured using fura-2. Riluzole (50–500 µmol/l) caused a rapid and sustained plateau increase in [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 in a concentration-dependent manner (EC 〈 sub 〉 50 〈 /sub 〉 = 150 µmol/l). The riluzole-induced rise in [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 was prevented by 58 and 20% by extracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 removal and nifedipine, respectively, but was not changed by La 〈 sup 〉 3+ 〈 /sup 〉 and verapamil. In Ca 〈 sup 〉 2+ 〈 /sup 〉 -free medium, thapsigargin, an inhibitor of the endoplasmic reticulum (ER) Ca 〈 sup 〉 2+ 〈 /sup 〉 -ATPase, caused a monophasic increase in [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 , after which the increasing effect of riluzole on [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 was attenuated by 84%; also, pretreatment with riluzole abolished the thapsigargin-induced [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 increase. U73122, an inhibitor of phospholipase C, abrogated the ATP (but not riluzole)-induced rise in [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 . A low concentration (6 µmol/l) of riluzole selectively potentiated the bradykinin (but not ATP and histamine)-induced increase in [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 . These results suggest that riluzole rapidly increases [Ca 〈 sup 〉 2+ 〈 /sup 〉 ] 〈 sub 〉 i 〈 /sub 〉 by stimulating both the extracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 influx via a nifedipine-sensitive pathway and intracellular Ca 〈 sup 〉 2+ 〈 /sup 〉 release from the ER via an as yet unidentified mechanism(s).
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000063798
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
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  • 9
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    Gambogic Acid Efficiently Kills Stem-Like Colorectal Cancer Cells by Upregulating ZFP36 Expression
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 46, No. 2 ( 2018), p. 829-846
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 46, No. 2 ( 2018), p. 829-846
    Abstract: Background/Aims: Gambogic acid (GA), the main active compound of Gamboge hanburyi, has been reported to be a potential novel antitumor drug. Whether GA inhibits putative cancer stem cells (CSCs), which are considered to be the major cause of cancer treatment failure, remains largely unknown. This study investigated whether GA inhibits the CSCs of colorectal cancer (CRC) and its possible mechanisms. Methods: We performed CCK8 and tumor sphere formation assays, percentage analysis of both side population and CD133+CD44+ cells, and the detection of stem cells markers, in order to assess the role of GA in inhibiting the stem celllike features of CRC. An mRNA microarray was performed to identify the downstream gene affected by GA and rescue assays were performed to further clarify whether the downstream gene is involved in the GA induced decrease of the stem cell-like CRC population. CRC cells were engineered with a CSC detector vector encoding GFP and luciferase (Luc) under the control of the Nanog promoter, which were utilized to investigate the effect of GA on putative CSC in human tumor xenograft-bearing mice using in vivo bioluminescence imaging. Results: Our results showed that GA significantly reduced tumor sphere formation and the percentages of side population and CD133+CD44+ cells, while also decreasing the expression of stemness and EMT-associated markers in CRC cells in vitro. GA killed stem-like CRC cells by upregulating the expression of ZFP36, which is dependent on the inactivation of the EGFR/ ERK signaling pathway. GFP+ cells harboring the PNanog-GFP-T2A-Luc transgene exhibited CSC characteristics. The in vivo results showed that GA significantly inhibited tumor growth in nude mice, accompanied by a remarkable reduction in the putative CSC number, based on whole-body bioluminescence imaging. Conclusion: These findings suggest that GA significantly inhibits putative CSCs of CRC both in vitro and in vivo by inhibiting the activation of the EGFR/ ERK/ZFP36 signaling pathway and may be an effective drug candidate for anticancer therapies.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000488740
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
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  • 10
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    Cord Blood Lysophosphatidylcholine 16: 1 is Positively Associated with Birth Weight
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 45, No. 2 ( 2018), p. 614-624
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 45, No. 2 ( 2018), p. 614-624
    Abstract: Background/Aims: Impaired birth outcomes, like low birth weight, have consistently been associated with increased disease susceptibility to hypertension in later life. Alterations in the maternal or fetal metabolism might impact on fetal growth and influence birth outcomes. Discerning associations between the maternal and fetal metabolome and surrogate parameters of fetal growth could give new insight into the complex relationship between intrauterine conditions, birth outcomes, and later life disease susceptibility. Methods: Using flow injection tandem mass spectrometry, targeted metabolomics was performed in serum samples obtained from 226 mother/child pairs at delivery. Associations between neonatal birth weight and concentrations of 163 maternal and fetal metabolites were analyzed. Results: After FDR adjustment using the Benjamini-Hochberg procedure lysophosphatidylcholines (LPC) 14: 0, 16: 1, and 18: 1 were strongly positively correlated with birth weight. In a stepwise linear regression model corrected for established confounding factors of birth weight, LPC 16: 1 showed the strongest independent association with birth weight (CI: 93.63 - 168.94; P = 6.94×10-11 ). The association with birth weight was stronger than classical confounding factors such as offspring sex (CI: -258.81- -61.32; P = 0.002) and maternal smoking during pregnancy (CI: -298.74 - -29.51; P = 0.017). Conclusions: After correction for multiple testing and adjustment for potential confounders, LPC 16: 1 showed a very strong and independent association with birth weight. The underlying molecular mechanisms linking fetal LPCs with birth weight need to be addressed in future studies.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000487118
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
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