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Results in Journal Naunyn-Schmiedeberg's Archives of Pharmacology: 23,805

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Rebecca Zehetbauer, Florentin von Haugwitz,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-12; https://doi.org/10.1007/s00210-021-02166-3

Abstract:
Motivated by the worldwide debate on gender equality, we analyzed the gender structure of the authors and the editorial board of Naunyn–Schmiedeberg’s Archives of Pharmacology. We wrote an algorithm to assign authors’ first names to a gender to determine the gender distribution of publications. We evaluated publications from German research institutes from 2000 to 2020. This resulted in a data set of 2929 authors. We could assign a first name to almost all authors. The percentage of female authors increased until 2008, but thereafter stagnated at around 30%. The position of senior author is far less often held by women (around 15%). Even though multiple political measures were implemented to increase the female participation, our analysis has shown no increase regardless. We also observed a strong decrease in German authorship (both male and female) since 2000. In the editorial board and for advisory editors, there has been a substantial increase in the proportion of women since 2016 as the result of appointments by the editor-in-chief. We discuss the strengths and limitations of our study in context with the literature and current developments in society and science and methodological pitfalls of studies in this field. More research is required to obtain a full picture of gender structure in science and to be able to properly interpret the data.
Yasin Bagheri, Saeed Sadigh-Eteghad, Ezzatollah Fathi, Javad Mahmoudi, Abdollah Abdollahpour, Nasim Jalili Namini, Zahra Malekinejad, Kiarash Mokhtari, Alireza Barati,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-10; https://doi.org/10.1007/s00210-021-02160-9

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Nilima Pradhan, Charan Singh,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2197-2222; https://doi.org/10.1007/s00210-021-02161-8

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Sheyda Houshmandfar, Ali Saeedi-Boroujeni, Mohammad Rashno, Ali Khodadadi,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2187-2195; https://doi.org/10.1007/s00210-021-02163-6

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Mehdi Sabzichi, Omolbanin Oladpour, Jamal Mohammadian, Mohsen Rashidi, Mahla Hosseinzadeh, Alireza Mardomi, Bahman Ramezani, Marjan Ghorbani, Fatemeh Ramezani
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-11; https://doi.org/10.1007/s00210-021-02164-5

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, Verena Ramirez Campos, Xiaoping Ning, Maurice T. Driessen, Lynda J. Krasenbaum, Karen Carr, Joshua M. Cohen
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2343-2346; https://doi.org/10.1007/s00210-021-02156-5

Abstract:
Recently, Gao et al. published an article titled “Monthly versus quarterly fremanezumab for the prevention of migraine: a systemic review and meta-analysis from randomized controlled trials” which concluded that monthly administration of fremanezumab led to significant reduction in monthly migraine days (MMD) when compared to quarterly fremanezumab. We have noted a critical flaw in Gao et al. meta-analysis wherein the authors have mistakenly utilized standard error values in place of standard deviation values in performing their pooled analyses. This error directly impacts the study results and conclusions. In this brief communication, we present revised analysis using correct methods. Using the correct SD values, our pooled analysis showed no significant difference in mean change from baseline in MMD between the two fremanezumab dosing regimens (P = 0.17). Furthermore, in the corrected subgroup analyses by type of migraine, there were no significant differences in mean change from baseline in MMD between monthly fremanezumab and quarterly fremanezumab (chronic migraine, P = 0.50; episodic migraine, P = 0.69). Overall, results from our corrected meta-analyses show that there is no significant difference in migraine prevention efficacy between monthly and quarterly fremanezumab dosing.
Gabriela Belen Martínez-Hernández, Enrique Jiménez-Ferrer, Manases González-Cortazar, Rubén Román-Ramos, Jaime Tortoriello, Gabriela Vargas-Villa,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-10; https://doi.org/10.1007/s00210-021-02155-6

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Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-18; https://doi.org/10.1007/s00210-021-02145-8

Abstract:
In the past, we generated transgenic mice that overexpress the human histamine 2 (H2)-receptor (H2-TG) or that overexpress the human serotonin 4 (5-HT4)-receptor (5-HT4-TG) in the heart. Here, we crossbred these lines of mice to generate double transgenic mice that overexpress both receptors (DT). This was done to study a conceivable interaction between these receptors in the mouse heart as a model for the human heart. When in left atria, initially, force of contraction was elevated maximally with 1 µM serotonin, and subsequently, histamine was cumulatively applied; a biphasic effect of histamine was noted: the force of contraction initially decreased, maximally at 10 nM histamine, and thereafter, the force of contraction increased again at 1 µM histamine. Notably, functional interaction between 5-HT and histamine was also identified in isolated electrically stimulated trabeculae carneae from human right atrium (obtained during cardiac surgery). These functional and biochemical data together are consistent with a joint overexpression of inotropically active H2-receptors and 5-HT4-receptors in the same mouse heart. We also describe an antagonistic interaction on the force of contraction of both receptors in the mouse atrium (DT) and in the human atrial muscle strips. We speculate that via this interaction, histamine might act as a “brake” on the cardiac actions of 5-HT via inhibitory GTP-binding proteins acting on the activity of adenylyl cyclase.
Agnès Bénardeau, Antje Kahnert, Tibor Schomber, Jutta Meyer, Mira Pavkovic, Axel Kretschmer, Bettina Lawrenz, Elke Hartmann, Ilka Mathar, Joerg Hueser, et al.
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-17; https://doi.org/10.1007/s00210-021-02149-4

Abstract:
Chronic kidney diseaQueryse (CKD) is associated with oxidative stress which can interrupt the nitric oxide (NO)/soluble guanylyl cyclase (sGC) signaling and decrease cyclic guanosine monophosphate (cGMP) production. Low cGMP concentrations can cause kidney damage and progression of CKD. The novel sGC activator runcaciguat targets the oxidized and heme-free form of sGC, restoring cGMP production under oxidative stress. The purpose of this study is to investigate if runcaciguat could provide an effective treatment for CKD. Runcaciguat was used for the treatment not only in rat CKD models with different etiologies and comorbidities, namely of hypertensive rats, the renin transgenic (RenTG) rat, and angiotensin-supplemented (ANG-SD) rat, but also in rats with diabetic and metabolic CKD, the Zucker diabetic fatty (ZDF) rat. The treatment duration was 2 to 42 weeks and runcaciguat was applied orally in doses from 1 to 10 mg/kg/bid. In these different rat CKD models, runcaciguat significantly reduced proteinuria (urinary protein to creatinine ratio; uPCR). These effects were also significant at doses which did not or only moderately decrease systemic blood pressure. Moreover, runcaciguat significantly decreased kidney injury biomarkers and attenuated morphological kidney damages. In RenTG rats, runcaciguat improved survival rates and markers of heart injury. These data demonstrate that the sGC activator runcaciguat exhibits cardio-renal protection at doses which did not reduce blood pressure and was effective in hypertensive as well as diabetic and metabolic CKD models. These data, therefore, suggest that runcaciguat, with its specific mode of action, represents an efficient treatment approach for CKD and associated CV diseases. Graphical abstract
Correction
, Aditi Budhauliya, Manu Jaggi, Anu T. Singh, Satyendra K. Rajput
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2349-2349; https://doi.org/10.1007/s00210-021-02150-x

Correction
Meng-Ting Li, Ya-Ya Du, Fei Zhong, Jie-Ru Wang, You-Wei Gu, Yue Zhang, Xuan-Tong Huang, Yi-Zhou Deng,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2347-2348; https://doi.org/10.1007/s00210-021-02138-7

, Hanan A. Farghaly, Yasmin A. Abdel-Wadood, Ghada A. Gomaa
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2167-2185; https://doi.org/10.1007/s00210-021-02154-7

The publisher has not yet granted permission to display this abstract.
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2153-2166; https://doi.org/10.1007/s00210-021-02144-9

Abstract:
The term “antibiotics” is a broadly used misnomer to designate antibacterial drugs. In a recent article, we have proposed to replace, e.g., the term “antibiotics” by “antibacterial drugs”, “antibiosis” by “antibacterial therapy”, “antibiogram” by “antibacteriogram”, and “antibiotic stewardship” by “antibacterial stewardship” (Seifert and Schirmer Trends Microbiol, 2021). In the present article, we show that many traditional terms related to antibiotics are used much more widely in the biomedical literature than the respective scientifically precise terms. This practice should be stopped. Moreover, we provide arguments to end the use of other broadly used terms in the biomedical literature such as “narrow-spectrum antibiotics” and “reserve antibiotics”, “chemotherapeutics”, and “tuberculostatics”. Finally, we provide several examples showing that antibacterial drugs are used for non-antibacterial indications and that some non-antibacterial drugs are used for antibacterial indications now. Thus, the increasing importance of drug repurposing renders it important to drop short designations of drug classes such as “antibiotics”. Rather, the term “drug” should be explicitly used, facilitating the inclusion of newly emerging indications such as antipsychotic and anti-inflammatory. This article is part of an effort to implement a new rational nomenclature of drug classes across the entire field of pharmacology.
Verena Kirsch,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2333-2341; https://doi.org/10.1007/s00210-021-02151-w

Abstract:
Although doctor-patient communication is essential for drug prescription, the literature reveals deficits in this area. An educational approach at the Cologne medical faculty aims at identifying and addressing those deficits in medical students. Fifth-year medical students first conducted a simulated prescription talk spontaneously. Subsequently, the conversation was discussed with peer students. A pharmacist moderated the discussion based upon a previously developed conversation guide. Afterwards, the same student had the conversation again, but as if for the first time. Conversations were video-recorded, transcribed and subjected to quantitative content analysis. Four days after the simulation, the students who conducted the talk, those who observed and discussed it, and students who did neither, completed a written test that focused on the content of an effective prescription talk. Content analysis revealed clear deficits in spontaneously led prescription talks. Even essential information as on adverse drug reactions were often lacking. Prescription talks became clearly more informative and comprehensive after the short, guided peer discussion. With regard to a comprehensive, informative prescription talk, the written test showed that both the students who conducted the talk and those who only observed it performed clearly better than the students who did not participate in the educational approach. Deficits regarding prescription talks are present in 5th year medical students. We provide an approach to both identify and address these deficits. It thus may be an example for training medical students in simulated and clinical environments like the EACPT recommended to improve pharmacology education.
Hamed Hajipour, Mohammad Nouri, Marjan Ghorbani, Ali Bahramifar, Reza Zolfaghari Emameh,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-10; https://doi.org/10.1007/s00210-021-02152-9

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Hamed Hajipour, Roshanak Sambrani, Marjan Ghorbani, Zahra Mirzamohammadi,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-9; https://doi.org/10.1007/s00210-021-02153-8

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Alireza Mardomi, Marzieh Ghollasi, Mohsen Korani, Mahsa Panahi, Mohammad Parsa-Kondelaji, Mehdi Sabzichi,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2309-2322; https://doi.org/10.1007/s00210-021-02134-x

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Ketren Carvalho Gomes, Francisco Wanderson Bizerra Lima, Helen Quézia Da Silva Aguiar, Suiane Silva de Araújo, Clarissa Amorim Silva de Cordova,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-19; https://doi.org/10.1007/s00210-021-02148-5

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Junchao Luo, Yin Zhang, Senbo Zhu, Yu Tong, Lichen Ji, Wei Zhang, Qiong Zhang,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 1991-2002; https://doi.org/10.1007/s00210-021-02131-0

Abstract:
The current understanding of osteoarthritis is developing from a mechanical disease caused by cartilage wear to a complex biological response involving inflammation, oxidative stress and other aspects. Nanoparticles are widely used in drug delivery due to its good stability in vivo and cell uptake efficiency. In addition to the above advantages, metal/metal oxide NPs, such as cerium oxide and manganese dioxide, can also simulate the activity of antioxidant enzymes and catalyze the degradation of superoxide anions and hydrogen peroxide. Degrading of metal/metal oxide nanoparticles releases metal ions, which may slow down the progression of osteoarthritis by inhibiting inflammation, promoting cartilage repair and inhibiting cartilage ossification. In present review, we focused on recent research works concerning osteoarthritis treating with metal/metal oxide nanoparticles, and introduced some potential nanoparticles that may have therapeutic effects.
Manja Newe, Theresa A. Kant, Maximilian Hoffmann, Johanna S. E. Rausch, Luise Winter, Karolina Künzel, Erik Klapproth, Claudia Günther,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2233-2244; https://doi.org/10.1007/s00210-021-02135-w

Abstract:
Skin fibrosis is a complex biological remodeling process occurring in disease like systemic sclerosis, morphea, or eosinophilic fasciitis. Since the knowledge about the underlying pathomechanisms is still incomplete, there is currently no therapy, which prevents or reverses skin fibrosis sufficiently. The present study investigates the role of polo-like kinase 2 (PLK2) and the pro-fibrotic cytokine osteopontin (OPN) in the pathogenesis of cutaneous fibrosis and demonstrates the antifibrotic effects of systemic mesalazine treatment in vivo. Isolated primary dermal fibroblasts of PLK2 wild-type (WT) and knockout (KO) mice were characterized in vitro. Skin thickness and histoarchitecture were studied in paraffin-embedded skin sections. The effects of mesalazine treatment were examined in isolated fibroblasts and PLK2 KO mice, which were fed 100 µg/g mesalazine for 6 months via the drinking water. Compared to WT, PLK2 KO fibroblasts displayed higher spontaneous myofibroblast differentiation, reduced proliferation rates, and overexpression of the fibrotic cytokine OPN. In vitro, 72 h of treatment with 10 mmol/L mesalazine induced phenotype conversion in PLK2 KO fibroblasts and attenuated OPN expression by inhibiting ERK1/2. In vivo, dermal myofibroblast differentiation, collagen accumulation, and skin thickening were prevented by mesalazine in PLK2 KO. Plasma creatinine levels indicated good tolerability of systemic long-term mesalazine treatment. The current study reveals a spontaneous fibrotic skin phenotype and ERK1/2-dependent OPN overexpression in PLK2 KO mice. We provide experimental evidence for the antifibrotic effectiveness of systemic mesalazine treatment to prevent fibrosis of the skin, suggesting further investigation in experimental and clinical settings.
Lihong Li, Man Yang, Chenyao Li,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-10; https://doi.org/10.1007/s00210-021-02133-y

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Tokiko Suzuki, Shigeyuki Yamashita, Kohshi Hattori, Naoyuki Matsuda, Yuichi Hattori
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2129-2139; https://doi.org/10.1007/s00210-021-02137-8

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Rasha M. S. M. Mohamed, Shimaa M. Elshazly, , Dalia M. Abd El Motteleb
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2117-2128; https://doi.org/10.1007/s00210-021-02130-1

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Fatemeh Yarmohammadi, Hedyieh Karbasforooshan, ,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2003-2011; https://doi.org/10.1007/s00210-021-02132-z

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Arthi Kumar, Sri Rahavi Boovarahan, Priyanka N. Prem, Meenakshi Ramanathan, David Raj Chellappan,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-13; https://doi.org/10.1007/s00210-021-02129-8

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Nasrin Dashti,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 1869-1878; https://doi.org/10.1007/s00210-021-02124-z

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Michal Weitman, Corina Bejar, Michal Melamed, Tehilla Weill, Inessa Yanovsky, Shani Zeeli, Abraham Nudelman,
Naunyn-Schmiedeberg's Archives of Pharmacology pp 1-13; https://doi.org/10.1007/s00210-021-02125-y

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Sutthiwan Janthamala, Apinya Jusakul, Sarinya Kongpetch, Phongsaran Kimawaha, Poramate Klanrit, Watcharin Loilome, Nisana Namwat, Anchalee Techasen
Naunyn-Schmiedeberg's Archives of Pharmacology; https://doi.org/10.1007/s00210-021-02123-0

Abstract:
Northeast Thailand has the highest incidence of cholangiocarcinoma (CCA) in the world. The lack of promising diagnostic markers and appropriate therapeutic drugs is the main problem for metastatic stage CCA patients who have a poor prognosis. N-cadherin, a cell adhesion molecule, is usually upregulated in cancers and has been proposed as an important mediator in epithelial-mesenchymal transition (EMT), one of the metastasis processes. Additionally, it has been shown that arctigenin, a seed isolated compound from Arctium lappa, can inhibit cancer cell progression via suppression of N-cadherin pathway. In this study, we investigated the protein expression of N-cadherin and its correlation with clinicopathological data of CCA patients, as well as the impact of arctigenin on KKU-213A and KKU-100 CCA cell lines and its underlying mechanisms. Immunohistochemistry results demonstrated that high expression of N-cadherin was significantly associated with severe CCA stage (p = 0.027), and shorter survival time (p = 0.002) of CCA patients. The mean overall survival times between low and high expression of N-cadherin were 31.6 and 14.8 months, respectively. Wound healing assays showed that arctigenin significantly inhibited CCA cell migration by downregulating N-cadherin whereas upregulating E-cadherin expression. Immunocytochemical staining revealed that arctigenin suppressed the expression of N-cadherin in both CCA cell lines. Furthermore, flow cytometry and western blot analysis revealed that arctigenin significantly reduced CCA cell viability and induced apoptosis via the Bax/Bcl-2/caspase-3 pathway. This research supports the use of N-cadherin as a prognostic marker for CCA and arctigenin as a potential alternative therapy for improving CCA treatment outcomes.
, Aditi Budhauliya, Manu Jaggi, Anu T. Singh, Satyendra K. Rajput
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 1815-1826; https://doi.org/10.1007/s00210-021-02088-0

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Antonio Wlisses da Silva, Maria Kueirislene A. Ferreira, Emanuela L. Rebouças, Francisco Rogenio S. Mendes, Atilano Lucas dos S. Moura, Jane Eire S. A. de Menezes, Márcia Machado Marinho, Emmanuel Silva Marinho, Hélcio S. Santos,
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2023-2032; https://doi.org/10.1007/s00210-021-02116-z

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, Fazal Subhan, Nazar Ul Islam, Muhammad Shahid, Naseem Ullah, , , Muhammad Usman Amin, Shehla Akbar, Ihsan Ullah, et al.
Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 2033-2047; https://doi.org/10.1007/s00210-021-02118-x

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Naunyn-Schmiedeberg's Archives of Pharmacology, Volume 394, pp 1633-1640; https://doi.org/10.1007/s00210-021-02120-3

Abstract:
Publications baring falsified and fabricated images appear frequently in the primary literature. Industrialized forms of image forgery as practiced by the so-called paper mills worsen the current situation even further. Good education and awareness within the scientific society are essential to create an environment in which honesty and trust are the prime values in experimental research. Here I focus on the detection of publication fraud and provide some examples and advice. Finally, my views on the future of fraud detection and prevention are given.
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