PReD-Bench/PRed-Bench huggingface dataset:
Extracellular calcium modulates brown adipocyte differentiation and identity
Authors: Ines Pramme-Steinwachs
Martin Jastroch
Siegfried Ussar
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Brown adipocytes; non-shivering thermogenesis; glucose; lipid homeostasis; metabolites
Affiliations: JRG Adipocytes & Metabolism, Institute for Diabetes & Obesity, Helmholtz Center Munich, 85748, Garching, Germany., German Center for Diabetes Research (DZD), 85764, Neuherberg, Germany., Institute for Diabetes & Obesity, Helmholtz Center Munich, 85748, Garching, Germany., JRG Adipocytes & Metabolism, Institute for Diabetes & Obesity, Helmholtz Center Munich, 85748, Garching, Germany. ., German Center for Diabetes Research (DZD), 85764, Neuherberg, Germany. .

Abstract:  Brown adipocytes are important in regulating non-shivering thermogenesis, whole body glucose and lipid homeostasis. Increasing evidence supports an important role of metabolites as well as macro- and micronutrients in brown adipocyte differentiation and function. Calcium is one of the most abundant ions in the body regulating multiple cellular processes. We observed that increasing extracellular calcium concentration during brown adipocyte differentiation blocks lipid accumulation and suppresses induction of major adipogenic transcription factors such as PPARγ and C/EBPα. In contrast, the depletion of calcium in the medium enhances adipogenesis and expression of brown adipocyte selective genes, such as UCP1. Mechanistically, we show that elevated extracellular calcium inhibits C/EBPβ activity through hyperactivation of ERK, a process that is independent of intracellular calcium levels and reversibly halts differentiation. Moreover, increased extracellular calcium solely after the induction phase of differentiation specifically suppresses gene expression of UCP1, PRDM16 and PGC1-α. Notably, depleting extracellular calcium provokes opposite effects. Together, we show that modulating extracellular calcium concentration controls brown adipocyte differentiation and thermogenic gene expression, highlighting the importance of tissue microenvironment on brown adipocyte heterogeneity and function. 

Retracted: No

PubPeer comments:
 Same blot differently labeled ![file] also in accompanying thesis ![file] , 
 Thank you very much for your interest in our study. In fact the membrane was incubated with both the Akt and Erk antibody simultaneously. Thus, the upper band corresponds to Akt as indicated by the box and the lower double band to Erk1 2. I hope that could clarify your comments, ,
Overexpression of human arginine decarboxylase rescues human mesenchymal stem cells against H₂O₂ toxicity through cell survival protein activation
Authors: Wonsuk Yang
Jong Eun Lee
Yu Mi Park
Won Taek Lee
Su Kyoung Seo
Kyung Ah Park
Journal: Journal of Korean Medical Science (2013)
Discipline: CLINICAL MEDICINE
Keywords: Arginine Decarboxylase; Cell Survival; Hydrogen Peroxide; Mesenchymal Stem Cells; Retroviral Vector.
Affiliations: Department of Anatomy, Yonsei University College of Medicine, Seoul, Korea., Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.

Abstract:  In this study, we explored the potentiality of human arginine decarboxylase (ADC) to enhance the survival of mesenchymal stem cells (MSCs) against unfavorable milieu of host tissues as the low survival of MSCs is the issue in cell transplantation therapy. To address this, human MSCs overexpressing human ADC were treated with H2O2 and the resultant intracellular events were examined. First, we examined whether human ADC is overexpressed in human MSCs. Then, we investigated cell survival or death related events. We found that the overexpression of human ADC increases formazan production and reduces caspase 3 activation and the numbers of FITC, hoechst, or propidium iodide positive cells in human MSCs exposed to H2O2. To elucidate the factors underlying these phenomena, AKT, CREB, and BDNF were examined. We found that the overexpression of human ADC phosphorylates AKT and CREB and increases BDNF level in human MSCs exposed to H2O2. The changes of these proteins are possibly relevant to the elevation of agmatine. Collectively, our data demonstrate that the overexpression of human ADC stimulates pro-survival factors to protect human MSCs against H2O2 toxicity. In conclusion, the present findings support that ADC can enhance the survival of MSCs against hostile environment of host tissues. 

Retracted: No

PubPeer comments:
 No arginine decarboxylase even exists in human or mammal(PMID: 19956990, https: www.ncbi.nlm.nih.gov gene ?term=AY325129). ,
A silver-impregnated antimicrobial dressing reduces hospital costs for pediatric burn patients
Authors: Dawn Adams
Heather N Paddock
Renata Fabia
Gail E Besner
John Hayes
Wendi Lowell
Shelia Giles
Journal: Journal of pediatric surgery (2007)
Discipline: CLINICAL MEDICINE
Keywords: novel silver-impregnated antimicrobial dressing; Aquacel Ag; hospital LOS; cost-effectiveness; Burn Registry Data

Abstract:  Purpose: Since using a novel silver-impregnated antimicrobial dressing (Aquacel Ag, ConvaTec, Princeton, NJ) in our pediatric patients with partial-thickness burns, hospital LOS has been significantly reduced. Here we investigated whether there was concomitant cost-effectiveness of this approach. Methods: We retrospectively reviewed Burn Registry Data from a large Children's Hospital Burn Unit from January 2005 through August 2005 for inpatients with partial-thickness burns treated with Aquacel Ag. A comparison group was composed of patients from the same period the previous year treated with silver sulfadiazine cream (SSD, Par Pharmaceuticals, Woodcliff, NJ) and matched for age and %TBSA burned. Patients with inhalation injury or full-thickness burns were excluded. Intent-to-treat analysis was limited to patients with less than 22% TBSA burn. Direct costs and total charges were compared statistically after log transformation due to the skewedness of the data. Results: Total charges and direct costs were significantly lower for Aquacel Ag-treated patients (n = 38) than for SSD-treated patients (n = 39) (P = .004 and P &lt; .001, respectively). In addition, Aquacel Ag-treated patients had a shorter LOS than SSD-treated patients. Discussion: These data strongly support our findings that the application of Aquacel Ag reduces hospital LOS which results in a significant cost savings in the care of pediatric patients with partial-thickness burns. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 #2 The comments is not correct! Just as one uses the thermometer to measure temperature, if you want to measure temperature, do you have to invent a new thermometer every time when you measure temperature? Do you have to invent a new ruler to measure the height of different person? The experiments published in JFM is the method for snow compaction. The method was used to estimate the permeability of goose down fiber, hope it is clear. , 
 #3 What ***P(max)*** is correct? **744 Pa?** OR **788 Pa?** , 
 #4 depends on the intitial permeability, the pressure build up is very sensitive to the initial permeability. Also, one need to understand 44 pa is like a slice of tissue in your hand, very minimum. happy to discuss. , 
 #5 You mean that a different initial condition (permeability) has yielded identical experimental results? ,
Differential modulation of transforming growth factor-betas and cyclooxygenases in the platelet lysates of male F344 rats by dietary lipids and piroxicam
Authors: Jayadev Raju
Ranjana P Bird
Journal: Molecular and Cellular Biochemistry (2002)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Platelets; chronic diseases; cancer; dietary fish oil; piroxicam
Affiliations: Department of Foods and Nutrition, University of Manitoba, Winnipeg, Canada.

Abstract:  Platelets are implicated in the pathogenesis of various chronic diseases including cancer. The main objective of the present study was to determine if dietary fish oil and piroxicam, known modulators of colon tumorigenesis, effect transforming growth factor (TGF)-betas and cyclooxygenase (COX) isozymes in the platelets of colon tumor-bearing male F344 rats. TGF-betas and COXs are important in the development of chronic illnesses including colon cancer. Animals harboring preneoplastic colonic lesions were randomly allocated to a low fat diet (5% by weight--low corn oil, LFC) and three high fat diets (23% by weight--high corn oil, HFC; high corn oil containing 150-ppm piroxicam, HFC+P; and high fish oil, HFF) for 16 weeks. TGF-beta1, TGF-beta2, COX-1 and COX-2 protein levels were assessed in the platelets by Western blot analysis. Active TGF-beta1 (12.5 kDa) level was significantly lower in the platelets of the HFC+P group (p &lt; 0.001), whereas precursor TGF-beta1 (39 kDa) level was significantly lower in the platelets of the HFF group (p &lt; 0.001). The anti-rabbit TGF-beta2 polyclonal antibody did not detect the 13-kDa active TGF-beta2 protein in the platelets. However a 29-kDa protein, potentially a precursor of TGF-beta2, was detected in the platelets of all the groups and was significantly lower in the HFC+P and HFF groups than in LFC and HFC (p &lt; 0.001). COX-1 level was significantly lower in the HFF group than the other three groups (p &lt; 0.001). COX-2 protein was detected in the platelets of all diet groups. Piroxicam in the presence of high corn oil (HFC+P) significantly lowered the level of COX-2 (p &lt; 0.001), without having any effect on COX-1 level. These findings conclusively show that LFC and HFC differ from HFF and HFC+P, and piroxicam differs from fish oil, in regulating the levels of TGF-betas and COX in the platelets. This supports the conjecture that the levels of bioactive constituents of the platelets are profoundly modulated by dietary lipids, which in turn could influence the pathogenesis of chronic illnesses. 

Retracted: No

PubPeer comments:
 Figure 3. * Pink, green, and blue boxes highlight bands that look similar to each other but presented in a different order between panels a) and b). Part of a set of 60+ papers reported to the journal in October 2015 with a friendly reminder in 2017. In the past five years, the journal did not correct or retract a single paper from this set. ![file] ,
Tumour suppressor PTEN enhanced enzyme activity of GPx, SOD and catalase by suppression of PI3K/AKT pathway in non-small cell lung cancer cell lines
Authors: Hakan Akca
Mutay Aslan
Aydin Demiray
Ibrahim Acikbas
Onur Tokgun
Journal: Journal of Enzyme Inhibition and Medicinal Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Phosphates; tensin homologue deleted on chromosome 10 (PTEN); tumour suppressor gene; phosphoinositol 3,4,5 triphosphates; PI3K/AKT pathway
Affiliations: Department of Medical Biology, School of Medicine, Pamukkale University, Denizli, Turkey. , Department of Medical Biology, School of Medicine, Pamukkale University,
Denizli, Turkey, Department of Biochemistry, School of Medicine, Akdeniz University,
Antalya, Turkey

Abstract:  Phosphates and tensin homologue deleted on chromosome 10 (PTEN) is a tumour suppressor gene which dephosphorilates phosphoinositol 3,4,5 triphosphates. Therefore PTEN can regulate PI3K/AKT pathway in cells. Because of promoter methylation or gene deletion, PTEN expression is commonly decreased or lost in non-small cell lung cancer (NSCLC) cell lines. Therefore, we hypothesized that PTEN could regulate the activity of superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx) and catalase. We first recreated PTENwt, G129R and G129E expressions in lung cell lines, in which endogenous PTEN expression was not detected. Then, we showed that PTEN could suppress AKT activity by its lipid phosphatase domain. We then examined the effect of recreated PTEN expressions in NSCLC cells. While PTENwt expression caused enhanced activity of SOD, GPx and catalase in transfected cells lines, neither G129R nor G129E expression effected enzyme activities. These results suggest that PTEN can up-regulate SOD, GPx and catalase activity by inhibition of PI3K/AKT pathway in NSCLC cell lines. 

Retracted: No

PubPeer comments:
 Figure 3. * Red boxes: The left PTEN and AKT panels appear to show partially overlapping blots. ![file] ,
mTORC2 phosphorylation of Akt1: a possible mechanism for hydrogen sulfide-induced cardioprotection
Authors: Yue Zhou
Daying Wang
Karsheng Lew
Peipei Wang
Arthur Mark Richards
Xiufang Gao
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Hydrogen sulfide; Akt activation; PI3K; mTORC2; PDK1
Affiliations: Cardiovascular Research Institute, National University of Singapore, Singapore, Singapore., Department of Cardiology, Putuo Hospital, Shanghai, China., Department of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.

Abstract:  Hydrogen sulfide (H2S) is known to have cardiac protective effects through Akt activation. Akt acts as a 'central sensor' for myocyte survival or death; its activity is regulated by multiple kinases including PI3K, mTORC2, PDK1 and phosphatases including PTEN, PP2A and PHLPPL. Based on the previous finding that PI3K inhibitor LY294002 abolishes H2S-induced Akt phosphorylation and cardioprotection, it is accepted that PI3K is the mediator of H2S-induced Akt phosphorylation. However, LY294002 inhibits both PI3K and mTOR, and PI3K only recruits Akt to the membrane where Akt is phosphorylated by Akt kinases. We undertook a series of experiments to further evaluate the role of mTORC2, PDK1, PTEN, PP2A and PHLPPL in H2S-induced Akt phosphorylation and cardioprotection, which, we believe, has not been investigated before. Hearts from adult Sprague-Dawley rats were isolated and subjected to (i) normoxia, (ii) global ischemia and (iii) ischemia/reperfusion in the presence or absence of 50 µM of H2S donor NaHS. Cardiac mechanical function and lactate dehydrogenase (LDH) release were assessed. All hearts also were Western analyzed at the end of perfusion for Akt and a panel of appropriate Akt regulators and targets. Hearts pretreated with 50 µM NaHS had improved function at the end of reperfusion (Rate pressure product; 19±4×10(3) vs. 10±3×10(3) mmHg/min, p&lt;0.05) and reduced cell injury (LDH release 19±10 vs. 170±87 mU/ml p&lt;0.05) compared to untreated hearts. NaHS significantly increased phospho-Akt, phospho-mTOR, phospho-Bim and Bcl-2 in reperfused hearts (P&lt;0.05). Furthermore using H9c2 cells we demonstrate that NaHS pretreatment reduces apoptosis following hypoxia/re-oxygenation. Importantly, PP242, a specific mTOR inhibitor, abolished both cardioprotection and protein phosphorylation in isolated heart and reduced apoptotic effects in H9c2 cells. Treating hearts with NaHS only during reperfusion produced less cardioprotection through a similar mechanism. These data suggest mTORC2 phosphorylation of Akt is a key mediator of H2S-induced cardioprotection in I/R. 

Retracted: No

PubPeer comments:
 Figures 5D (Pre-treatment) and 7D (post-treatment): * Red boxes: Lanes in the pAkt and t-Akt panels appear to look similar. Reported to the journal in October 2015, but no action taken as of today. ![file] ,
Inactivation of antibiotic-resistant bacteria by chlorine dioxide in soil and shifts in community composition
Authors: M S Wu
X Xu
Journal: RSC Advances (2019)
Discipline: CHEMISTRY
Keywords: Chlorine dioxide; antibiotic-resistant bacteria; soil; inactivation; dosage
Affiliations: College of Resources and Civil Engineering, Northeastern University, Shenyang 100819, China, School of Resources and Materials, Tongji Zhejiang College, Jiaxing

Abstract:  To study the efficacy of chlorine dioxide in the inactivation of antibiotic-resistant bacteria in soil, bacteria resistant to penicillin, amoxicillin or streptomycin were screened out from the soils around a hennery. The effects of dosage, contact time and pH value on the killing rates were investigated by batch experiments. The community composition before and after inactivation was analyzed by high-throughput genetic sequencing. The results showed that antibiotic-resistant bacteria are common and widespread in soil and the most resistant species is Staphylococcus aureus. More than 99% of antibiotic-resistant bacteria could be killed by chlorine dioxide at 5 mg L-1 within 30 min under neutral conditions. The killing log value declined slightly when the pH was changed from 4 to 9. The dominant genus was Sphingomonas, which was sensitive to chlorine dioxide and could be inactivated easily similar to Arthrobacter and Massilia. However, Micromonosporaceae and Thaumarchaeota were more resistant to chlorine dioxide than other species, and their relative abundance increased after disinfection. 

Retracted: No

PubPeer comments:
 **Thaumarchaeota*** are Archaea not Bacteria? Title: Inactivation of antibiotic-resistant **bacteria** by chlorine dioxide in soil and shifts in community composition Abstract To study the efficacy of chlorine dioxide in the inactivation of antibiotic-resistant **bacteria** in soil, bacteria resistant to penicillin, amoxicillin or streptomycin were screened out from the soils around a hennery... ...However, Micromonosporaceae and ***Thaumarchaeota*** were more resistant to chlorine dioxide than other species, and their relative abundance increased after disinfection. ,
HOTAIR contributes to the growth of liver cancer via targeting miR‑217
Authors: Xin-Ping Wang
Li-Ping Wang
Jun-Ping Wang
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: cell proliferation; cycle arrest; liver cancer; long non-coding RNA; microRNA-217.
Affiliations: Department of Medicine, Xi'an Honghui Hospital, Xi'an, Shaanxi 710068, P.R. China., Department of Medicine, The Friendship Hospital of Shaanxi, Xi'an, Shaanxi 710000, P.R. China., Department of General Surgery, Xi'an No. 4 Hospital, Xi'an, Shaanxi 710004, P.R. China.

Abstract:  Non-coding RNAs are important in the progression of liver cancer. The present study aimed to investigate the effects of long non-coding RNA HOX transcript antisense RNA (HOTAIR) on the proliferation of liver cancer and the association between HOTAIR and microRNA (miR)-217. It was demonstrated that the expression of HOTAIR was upregulated in liver cancer tissues and 3 liver cancer cell lines (MHCC97H, HepG2 and Hep3B). Inhibition of HOTAIR with HOTAIR small interfering (si) RNA lentiviral vectors significantly suppressed the cell proliferation of HepG2 cells, and downregulated the protein expression levels of two proliferation markers, Ki67 and proliferating cell nuclear antigen (PCNA). Furthermore, inhibition of HOTAIR induced G0/G1 cycle arrest by increasing the expression of p27 and decreasing the expression of cyclin D1. It was then predicted and verified that miR-217 was the target of HOTAIR. Expression of miR-217 was downregulated in liver cancer tissues and the 3 liver cancer cell lines. Further results revealed that inhibition of HOTAIR markedly upregulated the expression of miR-217 in HepG2 cells, and miR-217 inhibitor-induced reduction of miR-217 was significantly suppressed by HOTAIR inhibition. Furthermore, the increased cell proliferation and growth, the upregulated expression of Ki67 and PCNA, and the reduced G0/G1 cycle arrest induced by miR-217 inhibitor were partly rescued by inhibition of HOTAIR. Finally, the in vivo experiment indicated that HOTAIR inhibition suppressed tumorigenesis, including the smaller tumor volume and the reduced levels of Ki67. Overall, HOTAIR contributes to the proliferation and growth of liver cancer via downregulation of miR-217. 

Retracted: No

PubPeer comments:
 *[right]* Fig 5D:  The expression correlation between HOTAIR and mir-217 was determined in 25 liver cancer tissues . With its linearity, lack of noise and even distribution, the scatterplot looks more like someone s last-minute attempt to fake the homework for the physics experiment that they didn t perform, than any biological reality. It also shares a remarkable number of points in common with *[at left]* Fig 6D from [Li et al (2019)] . ![file] Dramatised here by superimposing 5D upon 6D. , 
 Fig 7G.  The expression of Ki67 and PCNA in primary tumor tissues was visualized by immunohistochemistry . Overlap marked. ![file] ,
Small Molecule Inhibitor C188-9 Synergistically Enhances the Demethylated Activity of Low-Dose 5-Aza-2'-Deoxycytidine Against Pancreatic Cancer
Authors: Linfeng Wu
Bei Sun
Shifeng Yang
Guangming Sun
Yilong Li
Fei Wang
Xina Li
Ping Xuan
Jisheng Hu
Rui Kong
Le Li
Journal: Frontiers in Oncology (2020)
Discipline: CLINICAL MEDICINE
Keywords: 5-aza-2′-deoxycytidine; C188-9; DNA methylation; RASSF1A; STAT3
Affiliations: Department of Pancreatic and Biliary Surgery, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China., Key Laboratory of Hepatosplenic Surgery, Ministry of Education, Harbin, China., School of Computer Science and Technology, Heilongjiang University, Harbin, China.

Abstract:  Aberrant DNA methylation, especially hypermethylation of tumor suppressor genes, has been associated with many cancers' progression. 5-Aza-2'-deoxycytidine (DAC) can reverse hypermethylation-induced gene silencing via regulating DNA methyltransferases (DNMTs) activity, In addition, low-dose of DAC was proved to exert durable antitumor effects against solid tumor cells. Nevertheless, no clinical effect of DAC has been made when fighting against pancreatic cancer. Hence, it is necessary to raise a novel therapeutic strategy that further enhance the efficacy of DAC but not increase side effect, which impede the utilization of DAC. In the present study, we have discovered that C188-9, a novel signal transduction activator of transcription (STAT) inhibitor, could improve the antitumor effects of low-dose DAC in vivo and in vitro. Further study demonstrated that such improvement was attributed to re-expression of Ras association domain family member 1A (RASSF1A), a well-known tumor suppressor gene. Bisulfite sequencing PCR (BSP) assay showed that C188-9 combined with DAC treatment could significantly reverse the hypermethylation status of RASSF1A promoter, which indicated that C188-9 could enhance the demethylation efficacy of DAC. Our data demonstrated that DNA methyltransferase 1 (DNMT1) was the underlying mechanism that C188-9 regulates the demethylation efficacy of DAC. Overall, these findings provide a novel therapeutic strategy combining low-dose DAC and C188-9 to improve therapeutic efficacy by inhibiting DNMT1-inducing promoter methylation. 

Retracted: No

PubPeer comments:
 Figure 2A appears to have some images which overlap. *** Closeup ![file] *** Showing labels ![file] ,
MRPS16 facilitates tumor progression via the PI3K/AKT/Snail signaling axis
Authors: Kang Wu
Xiaobing Long
Zhen Wang
Liwu Jiao
Minghui Zhou
Junjun Li
Journal: Journal of Cancer (2020)
Discipline: CLINICAL MEDICINE
Keywords: MRPS16; PI3K/AKT/Snail; glioma; invasion.
Affiliations: Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Street, Wuhan 430030, P.R. China., Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Street, Wuhan 430022, P.R. China., Department of Neurosurgery, The First People Hospital of Qujing, Qujing 655000, P.R. China.

Abstract:  Background: Although aberrant expression of MRPS16 (mitochondrial ribosomal protein S16) contributes to biological dysfunction, especially mitochondrial translation defects, the status of MRPS16 and its correlation with prognosis in tumors, especially glioma, which is a common, morbid and frequently lethal malignancy, are still controversial. Methods: Herein, we used high-throughput sequencing to identify the target molecule MRPS16. Subsequently, we detected MRPS16 protein and mRNA expression levels in normal brain tissue (NBT) and different grades of glioma tissue. The molecular effects of MRPS16 in glioma cells were tested by Western blotting, quantitative polymerase chain reaction (qRT-PCR), EdU, CCK-8, colony formation, Transwell migration and invasion assays. Results: Intriguingly, we found that MRPS16 knockdown suppressed tumor cell growth, migration and invasion. Conversely, MRPS16 over-expression increased tumor cell growth, migration and invasion. In addition, subsequent mechanistic studies indicated that MRPS16 promoted glioma cell growth, migration and invasion by the activating PI3K/AKT/Snail axis. Furthermore, we observed that the decrease in tumor cell growth, migration, invasion and Snail expression mediated by MRPS16 knockdown could be rescued by Snail over-expression. Conclusion: In short, our data demonstrate that MRPS16 over-expression remarkably promotes tumor cell growth, migration and invasion via the PI3K/AKT/Snail axis, which may be a promising prognostic marker for glioma. 

Retracted: No

PubPeer comments:
 There appear to be duplicated images in Fig. 3G. Could the authors please check? ![file] , 
 Dear Professor, First of all, thank you for your attention and valuable comments on this article. We re-examined this article and the original data carefully, and found that it was indeed the same picture that we used to make the mistake. Because we are not the same person in analyzing the data, writing the article, and making the picture, we apologize for the mistake. We will immediately contact the magazine editor to replace the entire picture. Best, thanks again for your correction. Regards, Kang Wu ,
Node of Ranvier as an Array of Bio-Nanoantennas for Infrared Communication in Nerve Tissue
Authors: Davide Micheli
Antonio Tozzi
Andrea Zangari
Roberta Galeazzi
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: Electromagnetic radiation; brain capabilities; visible spectrum; infrared spectrum; computational modelling
Affiliations: Azienda Ospedaliera San Camillo Forlanini, Pediatric Surgery and Urology Unit, Circonvallazione Gianicolense 87-00152, Roma, Italy., TIM S.P.A., Wireless Access Engineering Department, Viale Parco de' Medici, 61 - 00148, Roma, Italy. ., Dipartimento di Scienze della Vita e dell'Ambiente, università Politecnica delle Marche, via Brecce Bianche, 60131, Ancona, Italy., UOC Fisica Sanitaria, Azienda USL Toscana Sud Est, via Senese 161, 58100, Grosseto, Italy.

Abstract:  Electromagnetic radiation, in the visible and infrared spectrum, is increasingly being investigated for its possible role in the most evolved brain capabilities. Beside experimental evidence of electromagnetic cellular interactions, the possibility of light propagation in the axon has been recently demonstrated using computational modelling, although an explanation of its source is still not completely understood. We studied electromagnetic radiation onset and propagation at optical frequencies in myelinated axons, under the assumption that ion channel currents in the node of Ranvier behave like an array of nanoantennas emitting in the wavelength range from 300 to 2500 nm. Our results suggest that the wavelengths below 1600 nm are most likely to propagate throughout myelinated segments. Therefore, a broad wavelength window exists where both generation and propagation could happen, which in turn raises the possibility that such a radiation may play some role in neurotransmission. 

Retracted: No

PubPeer comments:
 This paper claims that sodium channels at the node of Ranvier are nano-antennae able to emit light which is then transmitted along the myelin-sheathed nerve acting as a sort of waveguide. I ll start a bit of reviewing: what mechanism would be driving alternating current through sodium channels at around 1e14 Hz, as would be required to operate the antennae at the frequency of visible light? ,
Aplasia Ras homolog member I expression induces apoptosis in renal cancer cells via the β-catenin signaling pathway
Authors: Zhen-Ming Jiang
Jian Yu
Chui-Ze Kong
Zhe Zhang
Bo Zhan
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: cancer; ARHI; renal; tumor suppressor gene; growth
Affiliations: Department of Urology, Institute of Urology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Abstract:  In numerous types of cancer, the Ras-associated tumor suppressor gene aplasia Ras homolog member I (ARHI), is downregulated. However, the function of ARHI in renal cancer remains to be elucidated. The present study investigated whether the suppressor gene ARHI influenced the growth of renal cancer cell lines and aimed to elucidate its mechanism of action, using the techniques of cell biology and molecular pathology. To the best of our knowledge, the present study was the first to determine the effects of ARHI on human renal cancer cells in vivo and in vitro. It was demonstrated that ARHI exhibited a tumor suppressor function in OS-RC-2 cells and acted via the β-catenin signaling pathway. It was additionally confirmed that the levels of ARHI messenger RNA and protein in renal cancer tissues were lower than those in matched normal tissues. These results provided a novel insight into the possible therapeutic applications of ARHI in renal cancer. 

Retracted: No

PubPeer comments:
 Table 1 lists the prescription for treating each syndrome of the infectious fever. ![file] Which authority recognizes the list of syndromes as in the first column? Which authority advises prescriptions as in the second column? References are missing for this info. ,
HS confers colonoprotection against TNBS-induced colitis by HO-1 upregulation in rats
Authors: Nikoletta Almási
Szilvia Török
Magdolna Kósa
Zoltán Baráth
Anikó Pósa
Zsolt Murlasits
Amin Al-Awar
János Nemcsók
Krisztina Kupai
Csaba Varga
Journal: Inflammopharmacology (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Colonoprotection; Gasotransmitter; Heme oxygenase-1; Hydrogen sulfide; TNBS.
Affiliations: Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726, Szeged, Hungary. ., Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726, Szeged, Hungary., Department of Pediatrics, Faculty of Medicine, University of Szeged, 6720, Szeged, Hungary., Department of Biology, J. Selye University, Komárno, Slovakia., College of Arts and Sciences, Sport Science Program, Qatar University, Doha, Qatar., Department of Orthodontics and Pediatric Dentistry, Faculty of Dentistry, University of Szeged, 6720, Szeged, Hungary.

Abstract:  Hydrogen sulfide (H2S) is an endogenous mediator that contributes to many important physiological processes including vasodilation and vascular smooth muscle relaxation; in turn, preventing tissue damage and reducing inflammation. Heme oxygenase (HO) enzymes, of which HO-1 is inducible by harmful stimuli, were found to regulate intestinal inflammation in experimental animal models of colitis. We aimed to investigate the protective effects of H2S against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats, and whether HO enzyme system is involved in the H2S-induced colonic cytoprotection. Male Wistar rats were treated with TNBS to induce colitis, and H2S donor (Lawesson's reagent) was prepared two times/day at different concentrations, and delivered per os (from day 1 to day 3). Our results suggest that daily treatment (2 times/day) with H2S donor, could significantly decrease the extent of colonic inflammation compared to vehicle treatment, and the most effective daily dose of H2S donor against inflammation was 18.75 µM/kg/day. Per os administration of H2S donor increased the colonic HO enzyme activity; on the contrary, the protective effect of H2S was abolished by the co-treatment with HO inhibitor. Our findings suggest that H2S confers colonoprotection, probably by modulation of anti-inflammatory parameters and HO enzyme activity. 

Retracted: No

PubPeer comments:
 Fig. 1 vs Fig. 5 https: imgur.com a qv0E4CA ,
Lasso Peptides: Heterologous Production and Potential Medical Application
Authors: Zi-Chun Hua
Cheng Cheng
Journal: Frontiers in Bioengineering and Biotechnology (2020)
Discipline: Multidisciplinary
Keywords: bioactivity; biosynthesis; heterologous expression; lasso peptides; medical application.
Affiliations: The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China., School of Biopharmacy, China Pharmaceutical University, Nanjing, China., Changzhou High-Tech Research Institute of Nanjing University, Changzhou, China., Jiangsu Target Pharma Laboratories Inc., Changzhou, China.

Abstract:  Lasso peptides are natural products found in bacteria. They belong to a specific family of ribosomally-synthesized and posttranslationally-modified peptides with an unusual lasso structure. Lasso peptides possess remarkable thermal and proteolytic stability and various biological activities, such as antimicrobial activity, enzyme inhibition, receptor blocking, anticancer properties and HIV antagonism. They have promising potential therapeutic effects on gastrointestinal diseases, tuberculosis, Alzheimer's disease, cardiovascular disease, fungal infections and cancer. Lasso peptides with high stability have been shown to be good carriers for other bioactive peptides. These make them attractive candidates for pharmaceutical research. This review aimed to describe the strategies used for the heterologous production of lasso peptides. Also, it indicated their therapeutical potential and their capacity to use as an efficient scaffold for epitope grafting. 

Retracted: No

PubPeer comments:
 This review has a sentence-by-sentence abridged version published a little earlier in Chinese. ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ,
From days to hours: Can MALDI-TOF MS system replace both conventional and molecular typing methods with new cut off level for Vancomycin Resistant Enterococcus faecium
Authors: Mehmet Parlak
Gulsen Hazirolan
Alper Karagoz
Sumeyra Savas
Journal: Journal of Microbiological Methods (2019)
Discipline: MICROBIOLOGY
Keywords: Identification; MALDI-TOF MS; Molecular typing; PFGE; VRE members.
Affiliations: The Scientific and Technological Research Council of Turkey, Kocaeli, Turkey. Electronic address: ., Department of Medical Microbiology, Hacettepe University School of Medicine, Ankara, Turkey., Turkey Public Health Agency, Ankara, Turkey., Department of Medical Microbiology, Yuzuncu Yil University School of Medicine, Ankara, Turkey.

Abstract:  Vancomycin-Resistant E. faecium (VRE) strains from clinical specimens were identified by conventional methods before. Following the phenotype-based identification, all strains were also identified using both BD Phoenix and VITEK MS bioMérieux System. Strains were typed with the Bruker MALDI-TOF MS system, pulsed field gel electrophoresis (PFGE) and 16S rRNA gene sequencing analysis and then the sensitivity compared for each. A cut off value of 850 assigned with Bruker MALDI-TOF MS system was found to give equal sensitivity to that of PFGE. Results obtained were compared with those of molecular typing. The main advantage of MALDI-TOF MS technology over the others was the much shorter analysis time which lasted only a few hours rather than days or a whole week. Also, the Bruker MALDI-TOF MS system was used for typing and compared with the gold standard method and this study is first to report the determined cut off level for typing of VRE strains. 

Retracted: No

PubPeer comments:
 ![file] The first PFGE dendrogram (a) is completely similar to that (b) published by Can et al. 2017. They both have common author. And the rest of the dendrogram is repetition of the band pattern. This band pattern is also smilar to previously published paper by Gu00fcldemir et al. 2015. These are different bacterial species and it is not possible to obtain smilar band pattern like that. Second paper (Can, H.Y. et al. (2017) Korean J. Food Sci. An. 37(2): 175-180.) Third paper (Gu00fcldmir et al. (2015) Turk Hij Den Biyol Derg, 72(1): 1-10.) ,
Qingyihuaji Formula Inhibits Pancreatic Cancer and Prolongs Survival by Downregulating Hes-1 and Hey-1
Authors: Yueqin Cai
Luming Liu
Yanli Xu
Shan Xu
Journal: Evidence-based Complementary and Alternative Medicine (2015)
Discipline: CLINICAL MEDICINE
Keywords: pancreatic cancer; Qingyihuaji formula; Notch signaling pathway; proliferation; survival
Affiliations: Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China., College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, China., Laboratory Animal Research Center, Zhejiang Chinese Medical University, Hangzhou 310053, China.

Abstract:  The dire prognosis of pancreatic cancer has not markedly improved during past decades. The present study was carried out to explore the effect of Qingyihuaji formula (QYHJ) on inhibiting pancreatic cancer and prolonging survival in related Notch signaling pathway. Proliferation of pancreatic cancer cells (SW1990 and PANC-1) was detected by MTT assay at 24, 48, and 72 h with exposure to various concentrations (0.08-50 mg/mL) of QYHJ water extract. Pancreatic tumor models of nude mice were divided into three groups randomly (control, QYHJ, and gemcitabine). mRNA and protein expression of Notch target genes (Hes-1, Hey-1, Hey-2, and Hey-L) in dissected tumor tissue were detected. Results showed that proliferation of SW1990 cells and PANC-1 cells was inhibited by QYHJ water extract in a dose-dependent and time-dependent manner. QYHJ effectively inhibited tumor growth and prolonged survival time in nude mice. Expression of both Hes-1 and Hey-1 was decreased significantly in QYHJ group, suggesting that Hes-1 and Hey-1 in Notch signaling pathway might be potential targets for QYHJ treatment. This research could help explain the clinical effectiveness of QYHJ and may provide advanced pancreatic cancer patients with a new therapeutic option. 

Retracted: Yes

PubPeer comments:
 Figure 6 appears to have some images which overlap. Roughly indicated in red and blue boxes. *** ![] , 
 Retraction Published 26 Feb 2021 Evidence-Based Complementary and Alternative Medicine has retracted the article titled u201cQingyihuaji Formula Inhibits Pancreatic Cancer and Prolongs Survival by Downregulating Hes-1 and Hey-1u201d [1], due to concerns identified with image overlap in Figure 6 as raised on PubPeer [2]. Figure 6(a) appears to have areas of overlap between the control and Gem panels. Figure 6(b) appears to have areas of overlap between the QYHJ and Gem panels. The authors were not able to provide a satisfactory response to these concerns and it is therefore being retracted with the agreement of the authors and the editorial board. ,
CAR T-cells targeting FLT3 have potent activity against FLT3−ITD+ AML and act synergistically with the FLT3-inhibitor crenolanib
Authors: Jordi Sierra
Halvard Bonig
Michael Hudecek
Thomas Nerreter
Hermann Einsele
Julian Rydzek
Hardikkumar Jetani
Irene Garcia-Cadenas
Simone Thomas
Javier Briones Meijide
Wolfgang Herr
Journal: Leukemia (2018)
Discipline: CLINICAL MEDICINE
Keywords: FLT3; chimeric antigen receptor; AML; T-cells; crenolanib
Affiliations: Medizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Würzburg, Germany., Hematology Department, Hospital de la Santa Creu i Sant Pau, Sant Pau and Jose Carreras Leukemia Research Institutes, Autonomous University of Barcelona, Barcelona, Spain., Klinik und Poliklinik für Innere Medizin III, Universitätsklinikum Regensburg, Regensburg, Germany., Institut für Transfusionsmedizin und Immunhämatologie, Goethe Universität Frankfurt, Frankfurt am Main, Germany., Deutsches Rotes Kreuz Blutspendedienst BaWüHe, Frankfurt, Germany., Medizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Würzburg, Germany. .

Abstract:  FMS-like tyrosine kinase 3 (FLT3) is a transmembrane protein expressed on normal hematopoietic stem and progenitor cells (HSC) and retained on malignant blasts in acute myeloid leukemia (AML). We engineered CD8+ and CD4+ T-cells expressing a FLT3-specific chimeric antigen receptor (CAR) and demonstrate they confer potent reactivity against AML cell lines and primary AML blasts that express either wild-type FLT3 or FLT3 with internal tandem duplication (FLT3-ITD). We also show that treatment with the FLT3-inhibitor crenolanib leads to increased surface expression of FLT3 specifically on FLT3-ITD+ AML cells and consecutively, enhanced recognition by FLT3-CAR T-cells in vitro and in vivo. As anticipated, we found that FLT3-CAR T-cells recognize normal HSCs in vitro and in vivo, and disrupt normal hematopoiesis in colony-formation assays, suggesting that adoptive therapy with FLT3-CAR T-cells will require subsequent CAR T-cell depletion and allogeneic HSC transplantation to reconstitute the hematopoietic system. Collectively, our data establish FLT3 as a novel CAR target in AML with particular relevance in high-risk FLT3-ITD+ AML. Further, our data provide the first proof-of-concept that CAR T-cell immunotherapy and small molecule inhibition can be used synergistically, as exemplified by our data showing superior antileukemia efficacy of FLT3-CAR T-cells in combination with crenolanib. 

Retracted: No

PubPeer comments:
 In figure 2a, there seems to be an image duplication: ![file] , 
 In Figure 4a, it seems like some areas in the  FLT3 CAR only have unnecessarily been covered with rectangles. It even seems like there was one more mouse on the right side, or is there another explanation for the grey shade (red dotted circle)? ![file] ,
Macrophagic myofasciitis and vaccination: consequence or coincidence?
Authors: Olinda Rebelo
Luís Negrão
Tânia Santiago
Anabela Matos
Journal: Rheumatology International (2015)
Discipline: CLINICAL MEDICINE
Keywords: Macrophagic myofasciitis; aluminum hydroxide; muscle lesions; long-term persistence; immunization
Affiliations: Rheumatology Unit, Centro Hospitalar e Universitário de Coimbra, Praceta Prof. Mota Pinto, 3000-075, Coimbra, Portugal, .

Abstract:  Macrophagic myofasciitis (MMF) characterized by specific muscle lesions assessing long-term persistence of aluminum hydroxide within macrophages at the site of previous immunization has been reported with increasing frequency in the past 10 years. We describe clinical and laboratory findings in patients with MMF. We did a retrospective analysis of 16 cases observed in our Neuropathology Laboratory, between January 2000 and July 2013. The mean age of the 16 patients was 48.8 ± 18.0 years; 80.0 % were female. Chronic fatigue syndrome was found in 8 of 16 patients. Half of the patients had elevated creatinine kinase levels, and 25.0 % had a myopathic electromyogram. Thirteen patients received intramuscular administration of aluminum-containing vaccine prior to the onset of symptoms. MMF may mirror a distinctive pattern of an inflammatory myopathy. The vaccines containing this adjuvant may trigger MMF in some patients. 

Retracted: No

PubPeer comments:
 Figure 1B. Each of the quadrants in each of the flow cytometry panels appears to show small repetitive areas. I have marked some of these repetitive areas with boxes of the same color. ![file] , 
 Figure 3B. *Turquoise panels: In the 4 days column, the SI and SD panels look unexpectedly similar. ![file] ,
Down-regulation of microRNA-21 reduces inflammation and podocyte apoptosis in diabetic nephropathy by relieving the repression of TIMP3 expression
Authors: Lei Zhao
Yanwei Xing
Bo Lin
Xiaoping Chen
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Diabetic nephropathy; High glucose; Streptozotocin; TIMP3; miR-21.
Affiliations: Department of Endocrinology, The First Affiliated Hospital of Henan University, Kaifeng, 475000, China., Basic Medical Sciences, Henan University, Kaifeng, 475004, China., Department of Pediatric, Kaifeng Hospital of TCM, Kaifeng, 475000, China., Basic Medical Sciences, Henan University, Kaifeng, 475004, China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. Concerns were raised about suspected duplicated features between the 'DN' and 'DN+anti-miR-NC' groups within Figure 2I, as detailed here: https://pubpeer.com/publications/FB14889727E5CF2651E012EEA10225#1. A journal investigation confirmed the presence of these suspected duplicated features. The journal asked the authors to provide an explanation to these concerns and the associated raw data. All authors were contacted on several occasions, but the journal did not receive a response. The Editor-in-Chief assessed the case and decided to retract the article. 

Retracted: No

PubPeer comments:
 In Figure 5, there is undeclared splicing of two WB lanes in the middle of membrane. ![file] ,
Metformin enhances the sensitivity of colorectal cancer cells to cisplatin through ROS-mediated PI3K/Akt signaling pathway
Authors: Surong Zhao
Hao Liu
Zongfen Shi
Xingyue Lu
Pei Zhang
Bing Zhu
Journal: Gene (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Apoptosis; Cisplatin; Colorectal cancer; Metformin; PI3K/Akt signaling pathway
Affiliations: School of Pharmacy, Bengbu Medical College, Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, Bengbu 233030, Anhui, China., School of Pharmacy, Bengbu Medical College, Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, Bengbu 233030, Anhui, China. Electronic address: ., Department of Gastrointestinal Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233000, Anhui, China. Electronic address: .

Abstract:  Metformin and cisplatin have been widely studied as antitumor agents. However, the effect of metformin combined with cisplatin has not been investigated in colorectal cancer (CRC) cells. This study was aimed to explore the effect of metformin or/and cisplatin on cell viability, apoptosis, and the related signaling pathways in CRC SW480 and SW620 cells. We found that metformin or cisplatin inhibited cell viability of SW480 and SW620 cells in a concentration- and time-dependent manner. Furthermore, metformin combined with cisplatin obviously inhibited cell viability, decreased colony formation, induced apoptosis, mediated cleavage of caspase-9, caspase-3 and PARP, activated mitochondrial membrane potential, downregulated Mcl-1 and Bcl-2 expression, upregulated Bak and Bax expression, and increased reactive oxygen species (ROS) production, compared to the individual agent in SW480 and SW620 cells, which were attenuated by N-acetyl-L-cysteine (NAC), a ROS scavenger. Moreover, NAC could recover the downregulation of p-PI3K and p-Akt treated with combination of metformin and cisplatin, which subsequently activated the PI3K/Akt signaling pathway. Taken together, our results demonstrated that metformin enhanced the sensitivity of CRC cells to cisplatin through ROS-mediated PI3K/Akt signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 2a contains two duplicated flow cytometry images with different Q1-Q4 values. ![file] ,