PReD-Bench/PRed-Bench huggingface dataset:
Zinc Supplementation and the Effects on Pregnancy Outcomes in Gestational Diabetes: a Randomized, Double-blind, Placebo-controlled Trial
Authors: Z Tabassi
N Talaee
M Karamali
Z Asemi
M Samimi
Z Heidarzadeh
H Bahardoost
S-M Seifati
Journal: Experimental and Clinical Endocrinology & Diabetes (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: zinc intake; inflammation; oxidative stress; pregnancy outcomes; gestational diabetes
Affiliations: Department of Gynecology and Obstetrics, School of Medicine, Iran University of Medical Sciences, Tehran, I.R. Iran, Department of Biology, Islamic Azad University, Ashkezar branch, Ashkezar, Iran, Department of Gynecology and Obstetrics, School of Medicine, Kashan University of Medical Sciences, Kashan, I.R. Iran, Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, I.R. Iran

Abstract:  Objective: The current study was designed to determine the beneficial effects of zinc intake on biomarkers of inflammation, oxidative stress, and pregnancy outcomes among pregnant women with gestational diabetes (GDM). Methods: This randomized, double-blind, placebo-controlled clinical trial was conducted among 50 women with GDM. Patients were randomly allocated to intake either 233 mg zinc gluconate (containing 30 mg zinc) (n=25) or a placebo (n=25) for 6 weeks. Fasting blood samples were taken at the fist of the study and after 6 weeks of intervention to quantify related variables. Newborn's weight, height, head circumference, Apgar score, and hyperbilirubinemia were determined. Results: The change in serum zinc levels after 6 weeks of supplementation was greater in women consuming zinc than in the placebo group (+8.5±13.5 vs. -3.6±16.2 mg/dL, P=0.006). Changes in serum high sensitivity C-reactive protein (hs-CRP) (-110.1±1 475.5 vs. +1 137.8±2 429.2 ng/mL, P=0.03) and plasma total antioxidant capacity (TAC) concentrations (+60.0±129.0 vs. -28.4±81.4 mmol/L, P=0.006) were significantly different between the supplemented women and placebo group. We did not find any significant effect of zinc administration on pregnancy outcomes. Conclusion: Taken together, zinc administration among patients with GDM was associated with decreased hs-CRP and increased TAC concentrations; however, it did not influence maternal plasma nitric oxide (NO), glutathione (GSH), malondialdehyde (MDA) levels, or pregnancy outcomes. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A64 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
RETRACTED: Possible involvement of the HMGB1/RAGE signaling mechanism in the induction of central post-stroke pain induced by acute global cerebral ischemia
Authors: Shogo Tokuyama
Keyue Liu
Shinichi Harada
Wataru Matsuura
Masahiro Nishibori
Journal: Brain Research (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Central post-stroke pain; Cerebral ischemia; High mobility group box-1; Receptor for advanced glycation end products.
Affiliations: Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, 1-1-3 Minatojima, Chuo-ku, Kobe 650-8586, Japan., Department of Pharmacology, Graduate School of Medicine, Dentistry and Pharmacological Sciences, Okayama University, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan., Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, 1-1-3 Minatojima, Chuo-ku, Kobe 650-8586, Japan. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Authors following an investigation into data manipulation (Figures 2A,B and 5) by an Investigation Committee at Kobe Gakuin University. Namely: Figures 2A and 2B - numerical disagreement (numbers removed) was found in some parts between the raw data and the article data, hence the significant difference illustrated in the published article was not obtained. Figure 5 - multiple numbers of the original raw data were changed, hence significant difference the significant difference illustrated in the published article was not obtained. 

Retracted: Yes

PubPeer comments:
 2021 retraction. https: www.sciencedirect.com science article pii S0006899321000652?via%3Dihub This article has been retracted at the request of the Authors following an investigation into data manipulation (Figures 2A,B and 5) by an Investigation Committee at Kobe Gakuin University. Namely: Figures 2A and 2B - numerical disagreement (numbers removed) was found in some parts between the raw data and the article data, hence the significant difference illustrated in the published article was not obtained. Figure 5 - multiple numbers of the original raw data were changed, hence significant difference the significant difference illustrated in the published article was not obtained. ,
CD206+ cell number differentiates influenza A (H1N1)pdm09 from seasonal influenza A virus in fatal cases
Authors: Heidi G Rodriguez-Ramirez
Lilia M Rangel-Martinez
Adrian G Rosas-Taraco
Luis Angel Ceceñas-Falcon
Mario C Salinas-Carmona
Oralia Barboza-Quintana
Americo Melo-de la Garza
Journal: Mediators of Inflammation (2014)
Discipline: IMMUNOLOGY
Keywords: influenza A (H1N1)pdm09; seasonal influenza virus; biomarkers; cytokines; cellular markers
Affiliations: Department of Immunology, School of Medicine and University Hospital, Universidad Autonoma de Nuevo Leon (UANL), Gonzalitos 235 Norte, Mitras Centro, 64460 Monterrey, NL, Mexico., Servicio de Anatomia Patologica y Citopatologia, School of Medicine and University Hospital, Universidad Autonoma de Nuevo Leon (UANL), Monterrey, NL, Mexico., Departamento de Anatomia Patologica, Instituto Mexicano del Seguro Social (IMSS), HGZ No. 6, San Nicolas de los Garza, NL, Mexico.

Abstract:  In 2009, a new influenza A (H1N1) virus affected many persons around the world. There is an urgent need for finding biomarkers to distinguish between influenza A (H1N1)pdm09 and seasonal influenza virus. We investigated these possible biomarkers in the lung of fatal cases of confirmed influenza A (H1N1)pdm09. Cytokines (inflammatory and anti-inflammatory) and cellular markers (macrophages and lymphocytes subpopulation markers) were analyzed in lung tissue from both influenza A (H1N1)pdm09 and seasonal influenza virus. High levels of IL-17, IFN-γ, and TNF-α positive cells were identical in lung tissue from the influenza A (H1N1)pdm09 and seasonal cases when compared with healthy lung tissue (P &lt; 0.05). Increased IL-4+ cells, and CD4+ and CD14+ cells were also found in high levels in both influenza A (H1N1)pdm09 and seasonal influenza virus (P &lt; 0.05). Low levels of CD206+ cells (marker of alternatively activated macrophages marker in lung) were found in influenza A (H1N1)pdm09 when compared with seasonal influenza virus (P &lt; 0.05), and the ratio of CD206/CD14+ cells was 2.5-fold higher in seasonal and noninfluenza group compared with influenza A (H1N1)pdm09 (P &lt; 0.05). In conclusion, CD206+ cells differentiate between influenza A (H1N1)pdm09 and seasonal influenza virus in lung tissue of fatal cases. 

Retracted: No

PubPeer comments:
null, 
 ![file] ,
RETRACTED ARTICLE: Optical rectification and absorption coefficients studied by a short-range topless exponential potential well with inverse square root
Authors: Meilin Hu
Qiucheng Yu
Kangxian Guo
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: Potential energy; Inverse square root; Schrödinger equation; Wave functions; Optical rectification
Affiliations: Department of Physics, School of Physics and Electronic Engineering, Guangzhou University, Guangzhou, 510006, China., Guangdong Provincial Engineering and Technology Research Center of Semiconductor Lighting and Backlighting, Guangzhou, 510006, China., Dipartimento di Fisica, Universitàdi Napoli Federico II, Complesso universitario di Monte Sant'Angelo, via Cintia, Napoli, 80126, Italy., Department of Physics, School of Physics and Electronic Engineering, Guangzhou University, Guangzhou, 510006, China. ., Guangdong Provincial Engineering and Technology Research Center of Semiconductor Lighting and Backlighting, Guangzhou, 510006, China. .

Abstract:  A topless potential energy with inverse square root is introduced to solve the energy spectrum equations and the bound state wave functions of the static Schrödinger equation by coordinate variation and combining the extraordinary coefficients of the confluent hypergeometric functions. Furthermore, the model of optical rectification (OR) and absorption coefficients (AC) with this special potential energy V(x) will appear regular changes. In this work, we explore the specific characteristics of the OR and AC with the inverse square root potential through multiple factors such as energy intervals and matrix elements. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: www.nature.com articles s41598-020-65240-5 Retraction of: Scientific Reports https: doi.org 10.1038 s41598-019-38519-5, published online 19 February 2019 The authors are retracting this Article. There is an error in the derivation described in the Article. Function z(x) as defined in the Article does not fulfil Eq. (5). This makes subsequent steps of the derivation incorrect. Additionally, the Article also states that Eq. (8) is a solution to Eq. (4). This too is incorrect. Overall, the authors are not able to guarantee the results and conclusions, and decided to retract the Article. All authors agree to retraction. ,
Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells
Authors: Tetsuro Matsumoto
Takakazu Sasaguri
Yoichi Ueta
Hiroshi Miyamoto
Masayoshi Nomura
Atsushi Mizokami
Shuji Harada
Naohiro Fujimoto
Journal: Cancer Investigation (2007)
Discipline: CLINICAL MEDICINE
Keywords: androgen-hypersensitivity; prostate cancer; AR coactivators; hormone-resistance; nuclear AR
Affiliations: Department of Urology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. 

Abstract:  Although androgen-hypersensitivity is one of the possible pathways of hormone-resistance in prostate cancer, the mechanisms of androgen-hypersensitivity are still largely unknown. Using androgen-hypersensitive prostate cancer cells LN-TR2, established from androgen-sensitive LNCaP cells by the long term treatment with tumor necrosis factor alpha, we explored the mechanisms of androgen-hypersensitivity in prostate cancer cells which may thus play a role in hormone-resistance. We examined the androgen receptor (AR) DNA sequence and the expression levels of AR and 8 AR cofactors in LNCaP and LN-TR2 cells. As a result, no novel mutation was developed in AR DNA in LN-TR2 cells. We observed higher expressions of nuclear AR upon androgen-treatment and 2 AR coactivators, ARA55 and TIF2, in LN-TR2 compared to LNCaP cells. An overexpression of ARA55 or TIF2 enhanced androgen-induced AR transcriptional activity in LNCaP cell. In the presence of those AR coactivators, AR activity was observed even at low concentrations of androgen. In 2 of 6 patients, the expression level of ARA55 was higher in cancer cells in hormone-resistant tumor than those in hormone-sensitive tumor. Taken together, our results suggest that prostate cancer cells change androgen-sensitivity by an overexpression of nuclear AR and AR coactivators, thus, resulting in transition from androgen-dependent to androgen-independent prostate cancer cells. An increase in nuclear AR and AR coactivators may cause androgen-hypersensitivity of prostate cancer cells and thus play a role in hormone-resistance, at least in some patients with prostate cancer. 

Retracted: No

PubPeer comments:
 Concern about similar looking lanes in Figures 2 and 3, reported to the journal in 2015. Boxes of the same color highlight lanes that look similar. ![file] ,
Kip/Cip and Ink4 Cdk inhibitors cooperate to induce cell cycle arrest in response to TGF-beta
Authors: I Reynisdóttir
K Polyak
A Iavarone
J Massagué
Journal: Genes & development (1995)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: G1 progression; cyclin D-dependent kinases; Cdk4; Cdk6; cyclin E-dependent kinase
Affiliations: Cell Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

Abstract:  G1 progression in mammalian cells requires the activity of the cyclin D-dependent kinases Cdk4 and/or Cdk6 and the cyclin E-dependent kinase Cdk2. Proliferating Mv1Lu mink lung epithelial cells and human keratinocytes contain high levels of the universal Cdk inhibitor p27Kip1 distributed in complexes with Cdk2, Cdk4, and Cdk6. Addition of the antimitogenic cytokine transforming growth factor-beta (TGF-beta) elevates expression of the Cdk4/6-specific inhibitor p15Ink4B and induces the release of p27 from Cdk4 and Cdk6. In Mv1Lu cells, this release of p27 coincides with increased binding of p27 to Cdk2. Recombinant p15 inhibits p27 binding to Cdk4 in vitro, and p15 overexpression induces the transfer of p27 from Cdk4 to Cdk2 in vivo, suggesting that the release of Cdk4-bound p27 in TGF-beta-treated cells is caused by the surge in p15 levels. In keratinocytes, TGF-beta increases not only p15 but also p21Cip1, which binds to Cdk2. These events correlate with Cdk2 inhibition and cell cycle arrest and occur without a loss of G1 Cdk components. The results suggest that TGF-beta induces G1 arrest in these two epithelial cell types by inhibiting various cyclin-Cdk kinases through the cooperative action of an Ink4 Cdk inhibitor and a Cip/Kip Cdk inhibitor. Subsequent to cell cycle arrest, Cdk2 and Cdk4 levels decline as part of a second set of events that may represent a program of cell adaptation to the quiescent state. 

Retracted: No

PubPeer comments:
 Fig 3B.  BX357664 inhibits cell proliferation and induces cell cycle arrest in the Caki-1 and Caki-2 cell lines. ...B. Flow cytometry analysis showed cell cycle arrest of Caki-1 and Caki-2 cells at the G1 phase after the overexpression of BX357664 . NC results are the same for Caki-1 and Caki-2. ![file] ,
Inhibitors of PARP-1 exert inhibitory effects on the biological characteristics of hepatocellular carcinoma cells in vitro
Authors: Zhongxia Yang
Haiyu Zhou
Xiaorong Mao
Liting Zhang
Ni Jiang
Xuebin Peng
Senrong Du
Journal: Molecular medicine reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: PARP-1 inhibitors; hepatocellular carcinoma; proliferation; apoptosis; migration
Affiliations: Department of Infectious Disease, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China., Department of Infectious Disease, Lanzhou Pulmonary Hospital, Lanzhou, Gansu 730046, P.R. China., Department of Orthopedics, The Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R. China.

Abstract:  It has been confirmed that the inhibitors of poly ADP-ribose polymerF(^9ase‑1 (PARP‑1) can inhibit the proliferation, apoptosis and invasion of tumor cells. However, the effects of inhibitors of PARP‑1 on hepatocellular carcinoma remain to be elucidated. The aim of the present study was to investigate the effect of three types of PARP‑1 inhibitor on the proliferation, apoptosis and migration of hepatocellular carcinoma in vitro. An MTT assay was performed to detect the proliferation of HepG2 cells following treatment with the PARP‑1 inhibitors, AG014699, BSI‑201 and AZD‑2281. Flow cytometry was used to detect the apoptosis of HepG2 cells, Western blot analysis was used to detect the protein expression of Casepase‑3, Casepase‑8, B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphatase and tensin homolog (PTEN), tissue inhibitor of metalloproteinase (TIMP) 3 and matrix metalloprotease (MMP) 3. A Transwell assay was performed to detect the migration of HepG2 cells. The results showed that AG014699, BSI‑201 and AZD‑2281 had an inhibitory effect on the proliferation of HepG2 cells in a time‑ and concentration‑dependent manner. AG014699 at concentrations of 10, 30 and 50 µmol/l, and BSI‑201 at concentrations of 20, 40 and 60 µmol/l induced the apoptosis of HepG2 cells, and the apoptotic rates were particularly high at 48 h (31, vs. 0.01%; P&lt;0.01 and 24.12, vs. 0.03%, respectively; P&lt;0.01). The protein expression levels of Caspase 3, Caspase 8, Bax, PTEN and TIMP 3 increased with increasing drug concentrations, whereas the protein levels of Bcl‑2 and MMP3 decreased with increasing drug concentrations, and were significantly different compared with those in the control group (P&lt;0.01). In conclusion, AG014699, BSI‑201 and AZD‑2281 inhibitors of PARP‑1 significantly inhibited the proliferation of HepG2 cells, however, AG014699 and BSI‑201 demonstrated more sensitivity, induced apoptosis and inhibited migration of the hepatocellular carcinoma cells, which may be associated with alterations of the apoptosis signaling pathway and the expression of proteins associated with migration. 

Retracted: No

PubPeer comments:
 Iniparib used in this study is NOT a PARP inhibitor and this has been known since 2012: https: clincancerres.aacrjournals.org content 18 2 510 https: clincancerres.aacrjournals.org content 18 6 1655 This study is therefor not valid. ,
Hamstring Eccentric Strengthening Program: Does Training Volume Matter?
Authors: Yannick Cholley
Gael Guilhem
Simon Avrillon
Martin Buchheit
Ben M Simpson
Mathieu Lacome
Journal: International Journal of Sports Physiology and Performance (2020)
Discipline: CLINICAL MEDICINE
Keywords: elite; injury management; microdosing; prevention; soccer.
Affiliations: 1 Performance Department, Paris Saint Germain, Saint-Germain-En-Laye, France., 2 French Institute of Sport (INSEP), Research Department, Laboratory Sport, Expertise and Performance (EA 7370).

Abstract:  Aim: To compare the effect of low versus high volume of eccentric-biased hamstring training programs on knee-flexor strength and fascicle length changes in elite soccer players. Methods: A total of 19 elite youth soccer players took part in this study and were randomly assigned into 2 subgroups. For 6 weeks in-season, the groups performed either a low-volume (1 set per exercise; 10 repetitions in total) or a high-volume (4 sets; 40 repetitions) eccentric training of their knee flexors. After 6-weeks midtraining (MID), players performed the alternate training regimen. Each training set consisted of 4 repetitions of the Nordic hamstring exercise and 6 repetitions of the bilateral stiff-leg deadlift. Eccentric knee-flexor strength (NordBord) as well as biceps femoris long head and semimembranosus fascicle length (scanned with ultrasound scanner) were assessed during pretraining (PRE), MID, and posttraining (POST) tests. Results: Knee-flexor eccentric strength very likely increased from PRE to MID (low volume: +11.3% [7.8%] and high volume: 11.4% [5.3%]), with a possibly-to-likely increase in biceps femoris long head (+4.5% [5.0%] and 4.8% [2.5%]) and semimembranosus (+4.3% [4.7%] and 6.3% [6.3%]) fascicle length in both groups. There was no substantial changes between MID and POST. Overall, there was no clear between-group difference in the changes from PRE to MID and MID to POST for neither knee-flexor eccentric strength, biceps femoris long head, nor semimembranosus fascicle length. Conclusions: Low-volume knee-flexor eccentric training is as effective as a greater training dose to substantially improve knee-flexor strength and fascicle length in-season in young elite soccer players. Low volume is, however, likely more appropriate to be used in an elite team facing congested schedules. 

Retracted: No

PubPeer comments:
 Figure 3B. Much more similar than expected. https: imgur.com Te97rvC ,
Herpes simplex virus disrupts NF-kappaB regulation by blocking its recruitment on the IkappaBalpha promoter and directing the factor on viral genes
Authors: Antonio Costanzo
Antonio Rossi
Carla Amici
Stefania Ciafrè
Massimo Levrero
Barbara Marinari
Mirna Balsamo
M Gabriella Santoro
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Herpes simplex viruses; IKK/NF-kappaB pathway; keratinocytes; signaling dysregulation; host-virus interaction
Affiliations: Department of Biology and Dermatology, University of Rome Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy.

Abstract:  Herpes simplex viruses (HSVs) are able to hijack the host-cell IkappaB kinase (IKK)/NF-kappaB pathway, which regulates critical cell functions from apoptosis to inflammatory responses; however, the molecular mechanisms involved and the outcome of the signaling dysregulation on the host-virus interaction are mostly unknown. Here we show that in human keratinocytes HSV-1 attains a sophisticated control of the IKK/NF-kappaB pathway, inducing two distinct temporally controlled waves of IKK activity and disrupting the NF-kappaB autoregulatory mechanism. Using chromatin immunoprecipitation we demonstrate that dysregulation of the NF-kappaB-response is mediated by a virus-induced block of NF-kappaB recruitment to the promoter of the IkappaBalpha gene, encoding the main NF-kappaB-inhibitor. We also show that HSV-1 redirects NF-kappaB recruitment to the promoter of ICP0, an immediate-early viral gene with a key role in promoting virus replication. The results reveal a new level of control of cellular functions by invading viruses and suggest that persistent NF-kappaB activation in HSV-1-infected cells, rather than being a host response to the virus, may play a positive role in promoting efficient viral replication. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
null, 
 Undeclared gel splicing site in Figure 6B. ![file] ,
Novel ORAI1 Mutation Disrupts Channel Trafficking Resulting in Combined Immunodeficiency
Authors: Fang Yu
Mehdi Adeli
Khaled Machaca
Rafah Mackeh
Bernice Lo
Nourhen Agrebi
Khadija KhudaBakhsh
Khaled Abouhazima
Amel Hassan
Journal: Journal of clinical immunology (2021)
Discipline: IMMUNOLOGY
Keywords: Ca2+ signaling; Combined immunodeficiency; ORAI1; anhidrosis; channel
Affiliations: Department of Physiology and Biophysics, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar., Calcium Signaling Group, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar., Translational Medicine Department, Sidra Medicine, Doha, Qatar., Pediatric Gastroenterology, Sidra Medicine, Education City, Doha, Qatar., General Pediatrics, Sidra Medicine, Education City, Doha, Qatar., Pediatric Allergy and Immunology Department, Sidra Medicine, Education City, Doha, Qatar., Translational Medicine Department, Sidra Medicine, Doha, Qatar. ., College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar. ., Pediatric Allergy and Immunology Department, Sidra Medicine, Education City, Doha, Qatar. ., Department of Physiology and Biophysics, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar. ., Calcium Signaling Group, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar. .

Abstract:  Store-operated Ca2+ entry (SOCE) represents a predominant Ca2+ influx pathway in non-excitable cells. SOCE is required for immune cell activation and is mediated by the plasma membrane (PM) channel ORAI1 and the endoplasmic reticulum (ER) Ca2+ sensor STIM1. Mutations in the Orai1 or STIM1 genes abolish SOCE leading to combined immunodeficiency (CID), muscular hypotonia, and anhidrotic ectodermal dysplasia. Here, we identify a novel autosomal recessive mutation in ORAI1 in a child with CID. The patient is homozygous for p.C126R mutation in the second transmembrane domain (TM2) of ORAI1, a region with no previous loss-of-function mutations. SOCE is suppressed in the patient's lymphocytes, which is associated with impaired T cell proliferation and cytokine production. Functional analyses demonstrate that the p.C126R mutation does not alter protein expression but disrupts ORAI1 trafficking. Orai1-C126R does not insert properly into the bilayer resulting in ER retention. Insertion of an Arg on the opposite face of TM2 (L135R) also results in defective folding and trafficking. We conclude that positive side chains within ORAI1 TM2 are not tolerated and result in misfolding, defective bilayer insertion, and channel trafficking thus abolishing SOCE and resulting in CID. 

Retracted: No

PubPeer comments:
 Is the high degree of similarity in the boxed regions expected for technical reasons? The samples are labelled Day 3 and Day 5 and the percentages are different. Please can the authors check? ![file] ,
Protective effect of Asarum sieboldii essential oil on ovalbumin induced allergic rhinitis in rat
Authors: Haoran Kang
Zhicheng Zhang
Journal: Bioscience reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Nasal mucosa; cytokines; histamine; nasal scratching; sneezing.
Affiliations: Department of Otorhinolaryngology, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, People’s Republic of China

Abstract:  Background: The study was aimed to investigate the protective effect of Asarum sieboldii Miq. essential oil (AEO) on ovalbumin (OVA)-induced allergic rhinitis (AR) in rats. Methods and results: Sixty Sprague-Dawley male rats were randomly divided into six groups (n=10): control, model, cetirizine (Cet, 4.65 g/kg), and AEO (0.5, 1.5, 3 g/kg) groups. All animals except the control group received repeated intranasal instillation with 20 μl of 20% OVA in Al(OH)3 saline solvent for 15 days. The control group was intranasally instilled with 5 mg/ml of Al(OH)3 instead of the same procedure. In the 15 days, Cet and AEO were orally administrated for 28 days. At the end of the drug administration, 20 μl of 5% OVA was given to animals to stimulate allergic reaction, then the rat behavioral detection, assessment of the patho-morphological changes in nasal mucosa, and the serum biomarkers were determined. The result showed that AEO could significantly reduce the amount of nasal secretions, sneezing, and the degree of nasal scratching in AR rats with EC50 = 1.5 and 2.8 g/kg, respectively. The degree of nasal mucosal inflammation in AEO group improved, the levels of immunoglobulin E (IgE), histamine, IL-4, IL-5, IL-17 were decreased, and the level of IFN-γ was increased obviously with EC50 = 2 g/kg. Conclusion: The study suggested that the possible mechanism might be related with the inhibition of histamine release and regulation of the cytokine levels, which plays an important role in the treatment of AR. 

Retracted: No

PubPeer comments:
 Figure 3D and 3E appear unexpectedly similar, given that the tissue is described as coming from two different animal groups. Yellow arrows in original. I also wish to note that the email address for the corresponding author does not seem to, um, correspond with their name. *** Closeup ![file] *** Figure 3 ![file] , 
 Figure 3C and 3D are also similar. See the post below http: pubpeer.com publications F9A6E3C845FDDEB030EE40D0EB8B93#1 , 
 https: doi.org 10.1042 BSR-20191370_EOC u201cThe Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates.u201d ,
Effects of huogu I formula (I) on correlated factors of bone regeneration in chickens with steroid-induced necrosis of femoral head
Authors: Rong Wan
Wei-heng Chen
Zhi-yao Wang
Chun-sheng Xiao
Xiang-ying Kong
He-ming Wang
Na Lin
Li Li
Journal: Chinese Journal of Integrative Medicine (2012)
Discipline: CLINICAL MEDICINE
Keywords: Huogu I formula; osteonecrosis; femoral head; bone morphogenetic protein-2 (BMP2); transforming growth factor beta1 (TGFβ(1))
Affiliations: Fujian University of Traditional Chinese Medicine, Fuzhou, China.

Abstract:  Objective: To study the mechanism of Huogu I formula (I) in treating osteonecrosis of femoral head. Methods: Forty-eight healthy female Leghorn chickens were randomly divided into control group, model group and Huogu I group, and each group consisted of 16 chickens. At the meantime of model establishment, chickens of the Huogu I group were administrated with decoction, while the model and control group with distilled water by gavage. At the 8th and 16th week after medication, blood samples were obtained for blood lipid detection while both sides of femoral head were harvested for the rest of examinations. Specifically, expressions of bone morphogenetic protein-2 (BMP2), transforming growth factor beta1 (TGFβ(1)), Smad4 and Smad7 were evaluated by immunohistochemistry, while expression of osteoprotegerin/receptor activator of nuclear factor kappaB ligand (OPG/RANKL) mRNA was detected by in situ hybridization. Results: Compared with the control group, serum levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) in the model group rose significantly. Positive cell counting of BMP2, TGFβ(1), Smad4 and OPG in femoral head of the model group dropped prominently. Positive cell counting of Smad7 and RANKL increased dramatically. In contrast with the model group, levels of TC, TG and LDL-C in Huogu I group reduced significantly. Positive cell counting of BMP2, TGFβ(1), Smad4 and OPG in femoral head of the Huogu I group increased prominently. Indices of Smad7 and RANKL both decreased significantly. Especially at the 8th week, these variations were more significant. Conclusion: Huogu I formula is effective in promoting repair of necrotic femoral head by regulating the expressions of BMP2, TGFβ(1), Smads and OPG/RANKL of osteoclast in femoral head. 

Retracted: No

PubPeer comments:
 Figure 3A. * Red boxes: In the lower row of panels, panel d (control group) and f (HG-I group) appear to show an overlap. ![file] ,
MicroRNA-326 inhibits cell proliferation and invasion, activating apoptosis in hepatocellular carcinoma by directly targeting LIM and SH3 protein 1
Authors: Yun Ran
Yongjian Xu
Yuncheng Zhang
Wenlin Chen
Shiping Hu
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocellular carcinoma; microRNA-326; cancer; diagnosis; therapy
Affiliations: Department of Hepatology, Longgang Hospital of Traditional Chinese Medicine, Shenzhen, Guangdong 518172, P.R. China.

Abstract:  Hepatocellular carcinoma (HCC) is the fifth-most common cancer and third leading cause of cancer-related deaths worldwide. Increasing evidence indicates that dysregulation of microRNAs is often observed in HCC, and has been extensively investigated in terms of cancer formation, progression, diagnosis, therapy, and prognosis. Recently, microRNA-326 (miR-326) has been demonstrated to play important roles in multiple types of human cancer. However, the expression pattern, clinical significance, roles and regulatory mechanisms of miR-326 in HCC have yet to be elucidated. In this study, miR-326 was frequently downregulated in HCC tissues and cell lines. Low miR-326 expression was significantly associated with the TNM stage, differentiation and lymph node metastasis of HCC patients. Further functional assays demonstrated that the recovered miR-326 expression inhibited HCC cell proliferation and invasion and activated cell apoptosis in vitro. In addition, LIM and SH3 protein 1 (LASP1) was identified as a direct target gene of miR-326 in HCC. Furthermore, LASP1 was upregulated in HCC tissues and cell lines. The expression level of LASP1 mRNA was inversely correlated with that of miR-326 in HCC tissues. Moreover, LASP1 silencing elicited effects similar to miR-326 overexpression on HCC cells, and LASP1 upregulation markedly reversed the effects of miR-326 overexpression on HCC cells. These results revealed that miR-326 suppressed the progression of HCC by directly targeting LASP1. Therefore, miR-326 may be used as a potential therapeutic target for the treatment of patients with HCC. 

Retracted: No

PubPeer comments:
 Figs 2E, 5E, 6E: ![] Orange box marks a panel shared with Figs 2D, 6D, 7D of [Deng et al (2018)] . ![] Here in context: ![] There may be other matches with other papers somewhere in this oeuvre. https: docs.google.com spreadsheets d 1X401JM6CcpTSkbKsPsOl20pRKQ-ns1S_J5pTwtBjqPw edit?usp=sharing , 
 *[above]* Fig 6D, and Fig 2D - flipped through 180 deg to facilitate comparison. *[below]* Fig 6C from  MicroRNAu2011337 inhibits colorectal cancer progression by directly targeting KRAS and suppressing the AKT and ERK pathways ([Liu et al 2017] ) **[retracted]**. ![file] ,
The mechanism of hsa-miR-424-5 combining PD-1 through mTORC signaling pathway to stimulate immune effect and participate in Type 1 diabetes
Authors: Tongyu Zhang
Yongxin Yan
Zhichen Zheng
Guofeng Wang
Journal: Bioscience reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: hsa-miR-424-5p; immune effect; mTORC signaling pathway; mechanism; signal molecule
Affiliations: Department of Endocrinology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, The First People's Hospital of Lianyungang, Lianyungang Clinical College of Nanjing Medical University, Lianyungang 222000, China., Department of Gastrointestinal Surgery, The Affiliated Lianyungang Hospital of Xuzhou Medical University, The First People's Hospital of Lianyungang, Lianyungang Clinical College of Nanjing Medical University, Lianyungang 222000, China.

Abstract:  In the present study, hsa-miR-424-5p mimic plasmid and hsa-mir-424-5p inhibitor plasmid were designed and injected into rats respectively, and miRNA control plasmid was also constructed. Models of Type 1 diabetes (T1D) were built. After successful modeling, the expression of hsa-miR-424-5p in lymphocytes was analyzed by RT-PCR. The expression of protein PD-1, T-bet, CXCR3, STING in Th1 lymphocytes and content of IGF-1 in islet tissue were analyzed by flow analysis. The protein levels of SHP2, Rheb, mTORC1, Rictor and Raptor in islet tissue were analyzed by Western blot. The results showed that hsa-miR-424-5p mimic group had the highest expression of hsa-miR-424-5p in lymphocytes. The expression of PD-1 was in hsa-miR-424-5p inhibitor &gt; miRNA control &gt; hsa-miR-424-5p mimic, while the expression of T-bet, CXCR3 and STING was in hsa-miR-424-5p mimic &gt; miRNA control &gt; hsa-miR-424-5p inhibitor. The expression of IGF-1 protein in hsa-miR-424-5p inhibitor group was the highest (32.08%) and hardly expressed in hsa-miR-424-5p mimic group (2.36%). The expression of SHP2, Rheb, mTORC1, Rictor and Raptor of insulin histoproteins were in hsa-miR-424-5p mimic group &gt; miRNA control of &gt; hsa-miR-424-5p inhibitor group, with statistical differences. It indicates that hsa-miR-424-5p binding PD-1 signaling molecules can stimulate the immune effect through the mTORC signaling pathway and participates in the pathogenesis of T1D. 

Retracted: No

PubPeer comments:
 The Western blot in figure 5 appears to have unidentified splices in some of the bands which are not apparent in all bands. Could the authors please post here the uncropped original scans? *** Enhanced contrast ![file] *** Figure 5 ![file] , 
 https: doi.org 10.1042 BSR-20193800_EOC The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Additive effects of eukaryotic co‑expression plasmid carrying GRIM‑19 and LKB1 genes on breast cancer in vitro and in vivo
Authors: Haipeng Liu
Wei Geng
Ying Shao
Duo Zhang
Ye Du
Wei Zhang
Tong Jiang
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: GRIM-19; LKB1; tumor suppressor gene; breast cancer; dual expression plasmid
Affiliations: Department of Cosmetology Plastic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Gastrointestinal Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China., Department of Neurological Surgery, The Second Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Abstract:  Gene associated with retinoid‑interferon‑induced mortality 19 (GRIM‑19) and the liver kinase B1 (LKB1) gene, two types of tumor suppressor gene, have been demonstrated to have important roles in breast carcinogenesis. The present study developed a dual expression plasmid that co‑expressed GRIM‑19 and LKB1, and evaluated the combined effects of the two genes against breast cancer in vitro and in vivo. Transfection with a plasmid for the simultaneous expression of GRIM‑19 and LKB1 (pGRIM19‑LKB1) into MCF‑7 breast cancer cells significantly inhibited the proliferation, colony formation, migration and invasion compared with the effects of transfection with either pGRIM‑19 or pLKB1 alone. Furthermore, transfection with pGRIM19‑LKB1 induced enhanced levels of apoptosis and cell cycle arrest at G0/G1 stage in MCF7 cells compared to the effects of pGRIM‑19 or pLKB1 alone. An in vivo experiment using an MCF‑7 xenograft tumor model demonstrated that intravenous injection of pGRIM19‑LKB1 had an enhanced effect on tumor growth inhibition compared to that of pGRIM‑19 or pLKB1 alone. In conclusion the findings of the present study suggested that transfection with eukaryotic plasmid for the simultaneous expression of GRIM‑19 and LKB1 more effectively suppressed the growth of breast cancer in vitro and in vivo, and may therefore have therapeutic potential for the treatment of human breast cancer. 

Retracted: Yes

PubPeer comments:
 Figs 4B, 1B.   ;  Western blotting assay was performed to determine the activation of STAT3 in T24 cells transfected with miR-195 mimics ;  Western blotting was performed to determine the protein level of Cdc42 in bladder cancer tissues (cancer) and their matched adjacent normal tissues (normal), as well as in bladder cancer T24 cells . ![file] I don t think these bands should share a lane in common. ,
Enhancement of Neural Stem Cells after Induction of Depression in Male Albino Rats (A histological & Immunohistochemical Study)
Authors: Mary Attia Morcos
Mohammad Deiaa Eldin Mohammad
Zeinab Mohamed Kamel Ismail
Alshaymaa Gamal Aboulkhair
Journal: International Journal of Stem Cells (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Depression; Neural Stem cells; Rhodiola rosea and Dentate gyrus.
Affiliations: Department of Histology, Faculty of Medicine, Cairo University, Cairo, Egypt.

Abstract:  Background and objectives: Depression is one of the most prevalent psychiatric disorders. Endogenous neural stem cells (NSCs) could replace damaged Hippocampal neurons in depression. This work was planned to evaluate Rhodiola rosea (Rr) extract possible role in stimulation of NSCs proliferation and in depression improvement. Methods and results: Thirty adult male albino rats were divided into three groups; control, untreated depressed model and Rr model. After depression induction by chronic mild stress, rats received Rr extract 1.5 g/kg/day for three weeks. The sucrose preference test (SP) was done before, after depression induction and 3 weeks after supplementation of Rr. The brain was removed and processed for H&amp;E and immunohistochemical staining for caspase 3, glial fibrillary acid protein (GFAP) and proliferating cell nuclear antigen (PCNA). Rr group revealed improved sucrose preference, increased undamaged neurons and decreased dark neurons. Moreover, Caspase 3 +ve cells were not detected, GFAP +ve cells increased and PCNA +ve cells were detected only in Rr group. Conclusions: This work points to the role of Rr in depression improvement and in stimulation of NSCs proliferation. 

Retracted: No

PubPeer comments:
 ![file] ,
PKCalpha activation downregulates ATM and radio-sensitizes androgen-sensitive human prostate cancer cells in vitro and in vivo
Authors: Susan A Rotenberg
Victor E Marquez
Jean-Philip Truman
Gabriel Lerman
Ji-Hye Kang
Adriana Haimovitz-Friedman
Richard Kolesnick
Zvi Fuks
Journal: Cancer biology & therapy (2009)
Discipline: CLINICAL MEDICINE
Keywords: Prostate cancer; PKCalpha; ATM; apoptosis; ceramide synthase
Affiliations: Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, Frederick, Maryland, USA.

Abstract:  We previously demonstrated that treatment of human androgen-responsive prostate cancer cell lines LNCaP and CWR22-Rv1 with 12-O-tetradecanoylphorbol 13-acetate (TPA), a known protein kinase C (PKC) activator, decreases ATM protein levels, thus de-repressing the enzyme ceramide synthase (CS) and promoting apoptosis as well as radio-sensitizing these cells.(1) Here we show that PKCalpha mediates the TPA effect on ATM expression, since ATM suppression and apoptosis induced by either TPA or diacylglycerol-lactone (DAG-lactone), both inducing PKCalpha activation,(2) are abrogated in LNCaP cells following transfection of a kinase-dead PKCalpha mutant (KD-PKCalpha). Similarly, KD-PKCalpha blocks the apoptotic response elicited by combination of TPA and radiation, whereas expression of constitutively active PKCalpha is sufficient to sensitize cells to radiation alone, without a need to pre-treat the cells with TPA. These findings identify CS activation as a downstream event of PKCalpha activity in LNCaP cells. Similar results were obtained in CWR22-Rv1 cells with DAG-lactone treatment. Using the LNCaP orthotopic prostate model it is shown that treatment with TPA or DAG-lactone induces significant reduction in tumor ATM levels coupled with tumor growth delay. Furthermore, while fractionated radiation alone produces significant tumor growth delay, pretreatment with TPA or DAG-lactone significantly potentiates tumor cure. These findings support a model in which activation of PKCalpha downregulates ATM, thus relieving CS repression by ATM and enhancing apoptosis via ceramide generation. This model may provide a basis for the design of new therapies in prostate cancer. 

Retracted: No

PubPeer comments:
 Figure 2A. Much more similar than you would expect. https: imgur.com xJoDcHD , 
 Figure 2A. Much more similar than you would expect. https: imgur.com chn806e ,
An androgen receptor-microrna-29a regulatory circuitry in mouse epididymis
Authors: Guangxin Yao
Yonglian Zhang
Shuanggang Hu
Xinxing Gao
Qiang Liu
Shengsong Xie
Jun Zhang
Wubin Ma
Minjie Ni
Xingxu Huang
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Androgen; Androgen Receptor; Epididymis; Gene Regulation; MicroRNA.
Affiliations: From the Shanghai Key Laboratory for Molecular Andrology, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Shanghai 200031, China.

Abstract:  MicroRNAs are involved in a number of cellular processes; thus, their deregulation is usually apt to the occurrence of diverse diseases. Previous studies indicate that abnormally up-regulated miR-29a is associated with several diseases, such as human acute myeloid leukemia and diabetes; therefore, the proper level of miR-29a is critical for homeostasis. Herein, we observed that miR-29a was repressed by androgen/androgen receptor signaling in mouse epididymis by targeting a conserved androgen response element located 8 kb upstream of miR-29b1a loci. It is well known that multiple regulatory programs often form a complicated network. Here, we found that miR-29a reversibly suppressed androgen receptor and its target genes by targeting IGF1 and p53 pathways. miR-29b1a-overexpressing transgenic mice displayed epididymis hypoplasia partially similar to the phenotype of those mice with an impaired androgen-androgen receptor signal system. Taken together, the results demonstrated that there is a regulatory circuitry between the androgen signaling pathway and miR-29a in mouse epididymis that may be vital for epididymal development and functions. 

Retracted: No

PubPeer comments:
 2 of the panels in Figure 4E are from the same image that has been cropped slightly differently ![file] , 
 there appears to be an undocumented splice in Figure 5B ![file] , 
 #2 Could that just be a scratch? , 
 #3 i d buy that , 
 #4 As would I. It would be nice, however, to have the authors respond to #1. ,
Exosomes secreted by chronic hepatitis B patients with PNALT and liver inflammation grade ≥ A2 promoted the progression of liver cancer by transferring miR‐25‐3p to inhibit the co‐expression of TCF21 and HHIP
Authors: Yi Ouyang
Wanfeng Wu
Shifang Peng
Xiaoyu Fu
Lei Fu
Yujing Tang
Deming Tan
Journal: Cell Proliferation (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CHB; HHIP; TCF21; exosome; liver cancer
Affiliations: Key Laboratory of Viral Hepatitis, Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, China., Department of Second Area of Liver Disease, Xia'men Hospital of Chinese Medicine, Xia'men, China., School of the Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, China.

Abstract:  Objectives: The current study aimed to investigate the mechanism by which exosomes secreted by CHB patients with PNALT and liver inflammation grade (≥A2) affected the development of liver cancer. Materials and methods: Gene expression was assessed by RT-PCR, Western blotting and immunohistochemistry. CCK-8, colony formation, transwell, scratch-wound and flow cytometry assays were used to detect cell viability, proliferation, apoptosis and metastasis. The interaction of TCF21 and HHIP was assessed by co-immunoprecipitation assay. Luciferase reporter was used to detect the combination of TCF21/HHIP and miR-25-3p. Xenograft studies in nude mice manifested tumour growth ability of miR-25-3p. Bioinformatics analyses were conducted using TargetScan, EVmiRNA, TCGA, GEO, DAVID, COEXPEDIA, UALCAN, UCSC and the Human Protein Atlas databases. Results: CHB-PNALT-Exo (≥A2) promoted the proliferation and metastasis of HepG2.2.15 cells. miR-25-3p was upregulated in CHB-PNALT-Exo (≥A2). miR-25-3p overexpression promoted cell proliferation and metastasis and was related to poor survival in patients with CHB-PNALT (≥A2). The cell proliferation- and metastasis-promoting functions of CHB-PNALT-Exo (≥A2) were abolished by miR-25-3p inhibitors. TCF21 directly interacted with HHIP. Inhibition of TCF21 or HHIP promoted cell proliferation and metastasis. Knockdown of TCF21 or HHIP counteracted the effects of CHB-PNALT-Exo (≥A2) containing miR-25-3p inhibitor on cell proliferation, metastasis and the expression of Ki67, E-cadherin and caspase-3/-9. Conclusions: Transfer of miR-25-3p by CHB-PNALT-Exo promoted the development of liver cancer by inhibiting the co-expression of TCF21 and HHIP. 

Retracted: No

PubPeer comments:
 Overlapping panels in Fig 2B. ![file] ,