PReD-Bench/PRed-Bench huggingface dataset:
45-Year Trends in Women’s Use of Time and Household Management Energy Expenditure
Authors: Steven N Blair
James R Hébert
Robin P Shook
Edward Archer
Diana M Thomas
Gregory A Hand
Carl J Lavie
Peter T Katzmarzyk
Kerry L McIver
Timothy S Church
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: socio-environmental factors; obesity; time-use; household management; energy expenditure
Affiliations: Department of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina, USA. 

Abstract:  Context: Relationships between socio-environmental factors and obesity are poorly understood due to a dearth of longitudinal population-level research. The objective of this analysis was to examine 45-year trends in time-use, household management (HM) and energy expenditure in women. Design and participants: Using national time-use data from women 19-64 years of age, we quantified time allocation and household management energy expenditure (HMEE) from 1965 to 2010. HM was defined as the sum of time spent in food preparation, post-meal cleaning activities (e.g., dish-washing), clothing maintenance (e.g., laundry), and general housework. HMEE was calculated using body weights from national surveys and metabolic equivalents. Results: The time allocated to HM by women (19-64 yrs) decreased from 25.7 hr/week in 1965 to 13.3 hr/week in 2010 (P&lt;0.001), with non-employed women decreasing by 16.6 hr/week and employed women by 6.7 hr/week (P&lt;0.001). HMEE for non-employed women decreased 42% from 25.1 Mj/week (6004 kilocalories per week) in 1965 to 14.6 Mj/week (3486 kcal/week) in 2010, a decrement of 10.5 Mj/week or 1.5 Mj/day (2518 kcal/week; 360 kcal/day) (P&lt;0.001), whereas employed women demonstrated a 30% decrement of 3.9 Mj/week, 0.55 Mj/day (923 kcal/week, 132 kcal/day) (P&lt;0.001). The time women spent in screen-based media use increased from 8.3 hr/week in 1965 to 16.5 hr/week in 2010 (P&lt;0.001), with non-employed women increasing 9.6 hr/week and employed women 7.5 hr/week (P&lt;0.001). Conclusions: From 1965 to 2010, there was a large and significant decrease in the time allocated to HM. By 2010, women allocated 25% more time to screen-based media use than HM (i.e., cooking, cleaning, and laundry combined). The reallocation of time from active pursuits (i.e., housework) to sedentary pastimes (e.g., watching TV) has important health consequences. These results suggest that the decrement in HMEE may have contributed to the increasing prevalence of obesity in women during the last five decades. 

Retracted: No

PubPeer comments:
 Figure 2 in this paper shows two flasks that look remarkably similar to flasks in Figure 1 of another paper by the same authors, i.e., Vundru Anil Kumar et al., IET Nanobiotechnol. (2016), doi: 10.1016 j.jphotobiol.2017.04.022 ![file] , 
 Dear Pubpeer Team, Thank you for identifying the error. We checked our raw data. We realized that the error was happened as the two experiments were performed at the same time. This was due to an oversight. Now the corrections are available https: doi.org 10.1016 j.jphotobiol.2021.112262 Thank you, ,
S100A8 contributes to drug resistance by promoting autophagy in leukemia cells
Authors: Liangchun Yang
Minghua Yang
Daolin Tang
Rui Kang
Yan Yu
Pei Zeng
Lizhi Cao
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Autophagy; S100A8; drug resistance; leukemia cells; chemotherapy
Affiliations: Department of Pediatrics, Xiangya Hospital, Central South University, Changsha Hunan, China., Department of Surgery, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, United States of America., Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Surgery, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, United States of America.

Abstract:  Autophagy is a double-edged sword in tumorigenesis and plays an important role in the resistance of cancer cells to chemotherapy. S100A8 is a member of the S100 calcium-binding protein family and plays an important role in the drug resistance of leukemia cells, with the mechanisms largely unknown. Here we report that S100A8 contributes to drug resistance in leukemia by promoting autophagy. S100A8 level was elevated in drug resistance leukemia cell lines relative to the nondrug resistant cell lines. Adriamycin and vincristine increased S100A8 in human leukemia cells, accompanied with upregulation of autophagy. RNA interference-mediated knockdown of S100A8 restored the chemosensitivity of leukemia cells, while overexpression of S100A8 enhanced drug resistance and increased autophagy. S100A8 physically interacted with the autophagy regulator BECN1 and was required for the formation of the BECN1-PI3KC3 complex. In addition, interaction between S100A8 and BECN1 relied upon the autophagic complex ULK1-mAtg13. Furthermore, we discovered that exogenous S100A8 induced autophagy, and RAGE was involved in exogenous S100A8-regulated autophagy. Our data demonstrated that S100A8 is involved in the development of chemoresistance in leukemia cells by regulating autophagy, and suggest that S100A8 may be a novel target for improving leukemia therapy. 

Retracted: Yes

PubPeer comments:
 This is an interesting report. Little detail is given about the mouse breeding, but I was surprised to see that these animals could be maintained given that the IMPC has reported both Male and Female infertility in animals lacking DUSP7 produced from their Dusp7tm1(KOMP)Wtsi reporter -tagged deletion allele (see https: www.mousephenotype.org data genes MGI:2387100 ) ,
Heme oxygenase 1 and renal ischemia and reperfusion injury: the impact of immunosuppressive drug
Authors: Vicente de Paula Antunes Teixeira
Georgia Daniela Macusso
Carolina Batista de Paula
Giselle Martins Gonçalves
Marcos Antônio Cenedeze
Carla Quarim Feitoza
Niels Olsen Saraiva Câmara
Marlene Antônia dos Reis
Alvaro Pacheco-Silva
Helady Sanders Pinheiro
Journal: International Immunopharmacology (2006)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Ischemia; reperfusion injury; acute renal failure; immunosuppressive drugs; acute graft dysfunction
Affiliations: Laboratório de Imunologia Clínica e Experimental, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil.

Abstract:  Ischemia and reperfusion injury (IRI) is the main etiology of acute renal failure in native and transplanted kidneys. In the transplantation field, immunosuppressive drugs may play an additional role in acute graft dysfunction. Acute cyclosporine nephrotoxicity (ATN) can result from vasoconstriction of the afferent arterioles, which may exacerbate deceased renal transplantation. HO-1 is a protective gene with anti-inflammatory and anti-apoptotic actions. We investigated whether HO-1 played a role in cyclosporine-induced renal dysfunction in an established model of IRI. Methods: Cyclosporine (100 mg/kg) was administered to mice before being subjected to 45 min of ischemia. Blood and kidney samples were collected at 24, 48 and 120 h after surgery. Acute tubular necrosis and tubular regeneration were quantified. HO-1 gene transcripts were amplified by real-time PCR. Results: Animals subjected to IRI presented with impaired renal function that peaked at 24 h (2.05 +/- 0.23 mg/dL), decreasing thereafter. Treatment with cyclosporine caused even more renal dysfunction at 48 h, sustained up to 120 h after reperfusion (1.53 +/- 0.6 mg/dL), when compared to the controls (0.63 +/- 0.09 mg/dL, p &lt; 0,05). Cyclosporine delayed tubular regeneration that was normally higher in controls at day 5 (67.0% vs. 37.6%, p &lt; 0.05). HO-1 was markedly up-regulated after IRI, and its expression was decreased by cyclosporine (2.06 folds). However, prior induction of HO-1 by cobalt protoporphyrin improved renal dysfunction. Conclusions: These results demonstrated that cyclosporine used in ischemic injured organs might also negatively affect post-transplantation recovery. 

Retracted: No

PubPeer comments:
 The abstract of this paper, including the key results, is almost identical to that of another paper (PMID 17003813). https: pubpeer.com publications 4D68CBF8C0488BCC28D3D89FB02297 ,
RETRACTED ARTICLE: Honokiol suppresses the development of post-ischemic glucose intolerance and neuronal damage in mice
Authors: Hwei-Hsien Chen
Mana Kobayashi
Kazuo Nakamoto
Ming-Huan Chan
Shogo Tokuyama
Maya Kishimoto
Wakako Fujita-Hamabe
Shinichi Harada
Journal: Journal of Natural Medicines (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Honokiol; Magnolia obovata; pharmacological effects; cerebral ischemia; glucose intolerance
Affiliations: Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Hyogo, Japan.

Abstract:  Honokiol, a constituent of Magnolia obovata, has various pharmacological effects, including protection against cerebral ischemia. However, few studies have been conducted to evaluate the possible neuroprotective effects of honokiol against cerebral ischemia. We recently reported that cerebral ischemic neuronal damage could be triggered by glucose intolerance that develops after the onset of ischemic stress (i.e., post-ischemic glucose intolerance). In addition, suppression of post-ischemic glucose intolerance significantly ameliorated ischemic neuronal damage. Here, we investigated the effects of honokiol on the development of post-ischemic glucose intolerance and neuronal damage. Mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. The development of post-ischemic glucose intolerance on day 1 and neuronal damage on day 3 after MCAO were significantly reduced by intraperitoneal administration of honokiol (10 mg/kg) compared with the vehicle-treated group. Honokiol did not affect serum insulin or adiponectin levels. However, honokiol significantly decreased the expression of phosphoenolpyruvate carboxykinase and increased the expression of 5'-AMP-activated protein kinase (AMPK) on day 1 after MCAO, compared with the vehicle-treated MCAO group. The results of this study suggest that honokiol could prevent post-ischemic glucose intolerance in an AMPK-dependent manner, which may be involved in the neuroprotective effects of honokiol against cerebral ischemia. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: link.springer.com article 10.1007%2Fs11418-011-0623-x#change-history 03 March 2020This article [1] has been retracted at the request of the corresponding author because an Investigation Committee established by Kobe Gakuin University (Kobe, Japan) has found numerous discrepancies between the raw data and the data presented in Figs.6b, d. Statistical analysis of the raw data showed no significant difference between conditions. Authors S. Harada, K. Nakamoto, W. Fujita-Hamabe, H.-H. Chen, M.-H. Chan, and S. Tokuyama agree with this retraction. Authors M. Kishimoto and M. Kobayashi could not be reached for comment about this retraction. ,
Myoferlin is a key regulator of EGFR activity in breast cancer
Authors: Agnès Noel
Arnaud Blomme
Vincent Hennequière
Philippe Delvenne
Akeila Bellahcène
Andrei Turtoi
Paul Peixoto
Elettra Bianchi
Eric Lifrange
Vincent Castronovo
Edwin De Pauw
Christine Gilles
Journal: Cancer research (2013)
Discipline: CLINICAL MEDICINE
Keywords: Myoferlin; cancer; breast cancers; epidermal growth factor receptor (EGFR); cell migration
Affiliations: Metastasis Research Laboratory, GIGA Cancer, University of Liège, Liège, Belgium. 

Abstract:  Myoferlin is a member of the ferlin family of proteins that participate in plasma membrane fusion, repair, and endocytosis. While some reports have implicated myoferlin in cancer, the extent of its expression in and contributions to cancer are not well established. In this study, we show that myoferlin is overexpressed in human breast cancers and that it has a critical role in controlling degradation of the epidermal growth factor (EGF) receptor (EGFR) after its activation and internalization in breast cancer cells. Myoferlin depletion blocked EGF-induced cell migration and epithelial-to-mesenchymal transition. Both effects were induced as a result of impaired degradation of phosphorylated EGFR via dysfunctional plasma membrane caveolae and alteration of caveolin homo-oligomerization. In parallel, myoferlin depletion reduced tumor development in a chicken chorioallantoic membrane xenograft model of human breast cancer. Considering the therapeutic significance of EGFR targeting, our findings identify myoferlin as a novel candidate function to target for future drug development. 

Retracted: No

PubPeer comments:
 Figure 3A and figure 3B use the same western-blot images with horizontal shift and in different conditions for one of them. ![file] , 
 Figure 6A uses the same western-blot image in several experimental conditions. MYOF western-blots in day 4 and 6 are the same. HSC70 in Myof siRNA at day 4 is the same than irrelevant siRNA at day 6. ![file] ,
TGF-β1 promotes cells invasion and migration by inducing epithelial mesenchymal transformation in oral squamous cell carcinoma
Authors: F Chen
J-Q Bu
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: TGF-β1; epithelial mesenchymal transition; invasion; oral squamous cell carcinoma; E-cadherin
Affiliations: Department of Stomatology, Chinese PLA General Hospital, Beijing, China. .

Abstract:  Objective: To investigate the role of TGF-β1 on epithelial mesenchymal transition (EMT) and invasion in oral squamous cell carcinoma cell line Tca8113. Materials and methods: Cultured Tca8113 cells were treated with different concentrations of TGF-β1 for 24 h. The morphological changes were observed under phase-contrast microscopy. The mRNA and protein expression levels of EMT relative marker E-cadherin and Vimentin were detected by RT-PCR and Western blot. The effect of TGF-β1 on migration and invasion ability of Tca8113 cells were detected using transwell method. Results: The results demonstrated that TGF-β1 could induce morphological changes in Tca8113 cells from epithelial to mesenchymal. The mRNA and protein level of epithelial marker E-cadherin was downregulated following treatment with TGF-β1, whereas the mRNA and protein expression level of mesenchymal marker protein Vimentin was upregulated. Furthermore, TGF-β1 significantly enhances the migration and invasiveness of Tca8113 cells, which were effectively reversed by TGF-β1 inhibitor, LY2109761 CONCLUSIONS: TGF-β1 enhances Tca8113 cells migration and invasion by inducing epithelial mesenchymal transition. 

Retracted: No

PubPeer comments:
  Figure 5. TGF-u03b21 promotes migration and invasion of Tca8113 cells. A.TGF-u03b21 promotes migration of Tca8113 cells (crystal violet stainingu00d7 200) (crystal violet stainingu00d7 200); B.TGF-u03b21 promotes invasion of Tca8113 cells (crystal violet stainingu00d7 200) (crystal violet stainingu00d7 200) . ![file] ,
Rainbow Trout IgM B Cells Preferentially Respond to Thymus-Independent Antigens but Are Activated by CD40L
Authors: Aitor G Granja
Alba Martín-Martín
Pedro Perdiguero
Irene Soleto
Carolina Tafalla
Patricia Díaz-Rosales
Journal: Frontiers in Immunology (2019)
Discipline: IMMUNOLOGY
Keywords: B cells; CD40L; IgM; extrafollicular responses; teleost fish.
Affiliations: Animal Health Research Center (CISA-INIA), Madrid, Spain.

Abstract:  In the absence of class switch recombination and germinal centers, the mechanisms through which B cells from teleost fish mount extrafollicular immunoglobulin M (IgM) memory responses remains mostly unexplored. In this report, we demonstrate that teleost IgM+ B cells respond to CD40L, a thymus-dependent activation signal, similarly to mammalian B2 cells. However, when stimulated with different types of antigens, fish IgM+ B cells only reach a general activation state in response to antigens cataloged as thymus-independent 1 (TI-1) in mammals, as established through both functional assays and RNA sequencing. Interestingly, fish IgM+ B cells remained completely unresponsive to TI-2 antigens, suggesting that the engagement of innate receptors provided by TI-1 antigens is required for the activation of teleost B cells. Finally, a synergy between CD40L and TI-1 antigens was also demonstrated, further supporting that there is no clear dichotomy between thymus-dependent and TI responses in teleost fish. 

Retracted: No

PubPeer comments:
 Figure 7 contains two duplicated FACS plots ![file] , 
 Its been a year, could the authors please also correct this obvious image duplication, as they in a similar case: https: pubpeer.com publications EB20B9F848F29C2A1FCD9ABFF4ECC8?utm_source=Safari utm_medium=BrowserExtension utm_campaign=Safari ,
S-adenosylmethionine-induced adipogenesis is accompanied by suppression of Wnt/β-catenin and Hedgehog signaling pathways
Authors: Meihua Jiang
Zuohua Liu
Wenjuan Sun
Tingting Ju
Jinxiu Huang
Yang Liu
Wentao Lv
Jingdong Yin
Feiyun Yang
Ling Xu
Boyang Yu
Defa Li
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: S-Adenosylmethionine; adipogenesis; skeletal muscle; differentiation; Wnt/β-catenin
Affiliations: State Key Laboratory of Animal Nutrition, College of Animal Science & Technology, China Agricultural University, Beijing, 100193, China, .

Abstract:  S-Adenosylmethionine (SAM) plays a crucial role as a methyl donor in various biological processes and has been previously shown to be involved in adipogenesis in skeletal muscle. This study was conducted to explore the mechanism of SAM inducing adipogenesis in skeletal muscle. Adipose precursor cells, 3T3-L1, and C2C12 cells, were induced into adipogenic differentiation by addition of SAM in MDI-differentiation media (0.5 mmol/L isobutylmethylxanthine, 1 μm/L dexamethasone, and 10 μg/mL insulin) to explore the role of SAM in promoting adipogenesis. Subsequently, cells were cultured with a medium containing SAM alone at the beginning of differentiation to test the relationship between SAM-induced adipogenesis and Wnt/β-catenin, and Hedgehog signaling pathways that control the cell commitment to adipogenic- or myogenic-differentiation. We found SAM possessed an additive effect with MDI in promoting adipogenesis of 3T3-L1 and C2C12 cells at the beginning of adipogenic differentiation. SAM could also individually induce cell adipogenesis in a dose-dependent manner. Moreover, the expression of Wnt/β-catenin and Hedgehog signals and their targets were suppressed by SAM (P &lt; 0.05). These results demonstrate that SAM, as an increasingly accepted nutritional supplement, can initiate adipogenesis of adipose precursor cells derived from adipose and muscle tissues, a function at least partly correlated with the suppression of Wnt/β-catenin and Hedgehog pathways. 

Retracted: No

PubPeer comments:
 Figure 5: Magenta rectangles show duplicated images. Would the authors please comment? ![file] , 
 The boxes that have been added to show which areas are magnified haven t been positioned very carefully, this makes the images more difficult to interpret. For example, Figure 6, I placed the magenta box, the author s black box borders the wrong area. ![file] ,
Endoplasmic reticulum stress induces apoptosis by an apoptosome-dependent but caspase 12-independent mechanism
Authors: Elisabetta Ferraro
Tilmann Achsel
Francesco Cecconi
Mauro Piacentini
Roberta Tufi
Federica Di Sano
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Endoplasmic reticulum; unfolded protein response; apoptotic program; ER calcium stores; apoptosome
Affiliations: Department of Biology, University of Tor Vergata.

Abstract:  The endoplasmic reticulum (ER) is the cellular site of polypeptide folding and modification. When these processes are hampered, an unfolded protein response (UPR) is activated. If the damage is too broad, the mammalian UPR launches the apoptotic program. As a consequence, mobilization of ER calcium stores sensitizes mitochondria to direct proapoptotic stimuli. We make use of a mouse Apaf1-deficient cell system of proneural origin to understand the roles played in this context by the apoptosome, the most studied apoptotic machinery along the mitochondrial pathway of death. We show here that in the absence of the apoptosome ER stress induces cytochrome c release from the mitochondria but that apoptosis cannot occur. Under these circumstances, Grp78/BiP and GADD153/CHOP, both hallmarks of UPR, are canonically up-regulated, and calcium is properly released from ER stores. We also demonstrate that caspase 12, a protease until now believed to play a central role in the initiation of ER stress-induced cell death in the mouse system, is dispensable for the mitochondrial pathway of death to take place. 

Retracted: No

PubPeer comments:
 Fig. 1A u2013 more similar than expected (in red). Could authors check it please? ![file] ,
Favorable effects of vitamin D supplementation on pregnancy outcomes in gestational diabetes: a double blind randomized controlled clinical trial
Authors: Z Asemi
A Esmaillzadeh
M Karamali
Journal: Hormone and Metabolic Research (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Gestational diabetes mellitus; vitamin D deficiency; pregnancy outcomes; vitamin D supplementation; randomized controlled trial
Affiliations: Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, I. R. Iran., Department of Gynecology and Obstetrics, School of Medicine, Arak University of Medical Sciences, Arak, I. R. Iran., Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, I. R. Iran.

Abstract:  Gestational diabetes mellitus (GDM) has been recognized as a significant risk factor for unfavorable pregnancy outcomes. Prevalence of vitamin D deficiency is highly prevalent among women with GDM. This study was designed to assess the effect of vitamin D supplementation on pregnancy outcomes of pregnant women with GDM who were not on oral hypoglycemic agents. This randomized controlled clinical trial was performed among 45 pregnant women diagnosed with GDM at 24-28 weeks' gestation. Subjects were randomly assigned to consume either vitamin D supplements (cholecalciferol) or placebo. Individuals in the vitamin D group (n=22) received 50 000 IU vitamin D3 pearl 2 times during the study: at study baseline and day 21 of intervention and those in placebo group (n=23) received 2 placebos at the mentioned times. Fasting blood samples were taken at baseline to measure fasting plasma glucose. Participants underwent a 3-h oral glucose tolerance tests (OGTT) and the blood samples were collected at time 60, 120, and 180 min to measure plasma glucose levels. Newborn's weight, height, head circumference, Apgar score, and hyperbilirubinemia were determined. Taking vitamin D supplements, compared with placebo, resulted in improved pregnancy outcomes; such that those in the vitamin D group had no case of polyhydramnios, while 17.4% of subjects in placebo group had this condition (p=0.04). In addition, newborn's hyperbilirubinemia was significantly lower in vitamin D group than that in placebo group (27.3% vs. 60.9%, p=0.02). In conclusion, vitamin D supplementation for 6 weeks among pregnant women with GDM resulted in decreased maternal polyhydramnios and infant hyperbilirubinemia compared with placebo. Clinical trial registration number www.irct.ir:IRCT201305115623N7. 

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 A30 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 ,
Theory of mind impairment in Huntington's disease patients and their relatives
Authors: Yaneth Rodríguez-Agudelo
Leo Bayliss
Mireya Chávez-Oliveros
Víctor Galvez
Marie Catherine Boll
Guillermo Delgado-García
Adriana Ochoa-Morales
Journal: Arquivos de Neuro-Psiquiatria (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Huntington disease; Theory of mind; ToM deficits; Cognitive impairment; Movement disorders
Affiliations: Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Division of Neurology, Mexico City, Tlalpan, Mexico., Universidad Panamericana, Escuela de Psicologia, Laboratorio de Neurociencias Cognitivas y Desarrollo, Mexico City, Mexico., Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Division of Genetics and Molecular Biology, Mexico City, Tlalpan, Mexico., Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Department of Neuropsychology and Support Groups, Mexico City, Tlalpan, Mexico., Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Clinical Research Laboratory, Mexico City, Tlalpan, Mexico.

Abstract:  Huntington disease (HD) is an autosomal dominant genetic disorder characterized by movement disorders, cognitive impairment, and psychiatric symptoms. Relatives of HD patients experience a great burden as the latter suffer from altered social conduct and deterioration of interpersonal relationships. Theory of mind (ToM) is the ability to attribute mental states (to oneself and others). Deficits in ToM are thought to have a role in the changes in empathy and interpersonal difficulties that HD patients face. METHODS We conducted a cross sectional study to compare ToM task scores of patients with mild to moderate HD, their relatives (spouse or at-risk first-degree relative with a negative gene test) and controls.Individuals with dementia or depression were excluded. The ToM test battery included Spanish versions of the Reading Mind in the Eyes Test (RMET), Happé's Strange Stories (Social and Physical Stories subtests) and the Hinting Task. RESULTS The series comprised 12 HD patients, 12 relatives and 12 controls. The HD patients showed lower affective ToM scores than controls (RMET 19 [3.5] vs 23.9 [2.7], p = 0.016). Cognitive ToM tasks scores were lower in HD patients than controls as well (Happé's Social Stories 9 [2.6] vs 13 [1.9], p = 0.001; the Hinting Task 13.6 [3.4] vs 17.5 [4.0], p = 0.009). In the Hinting Task, HD relatives had lower scores in than controls (13 [3.2] vs 17.5 [4.0], p = 0.009) and similar scores to controls in the rest of the battery. CONCLUSION The HD patients with mild to moderate disease severity and their relatives show ToM deficits. 

Retracted: No

PubPeer comments:
 Would you consider changing a couple of word in the introduction? ![file] ![file] ,
Novel preparation method for sustained-release PLGA microspheres using water-in-oil-in-hydrophilic-oil-in-water emulsion
Authors: Weien Yuan
Zhenguo Liu
Liangming Wei
Yinghui Chen
Liuqing Ma
Xiaoyun Hong
Journal: International Journal of Nanomedicine (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microspheres; protein; sustained-release; water-in-oil-in-hydrophilic oil-in-water emulsion.
Affiliations: Department of Neurology, Xinhua Hospital affiliated to Shanghai JiaoTong University, School of Medicine, Shanghai, People's Republic of China.

Abstract:  An increasing number of drugs are needing improved formulations to optimize patient compliance because of their short half-lives in blood. Sustained-release formulations of drugs are often required for long-term efficacy, and microspheres are among the most popular ones. When drugs are encapsulated into microsphere formulations, different methods of preparation need to be used according to specific clinical requirements and the differing physicochemical characteristics of individual drugs. In this work, we developed a novel method for sustained-release drug delivery using a water-in-oil-in-hydrophilic oil-in-water (w/o/oh/w) emulsion to encapsulate a drug into poly(lactic-co-glycolic acid) (PLGA) microspheres. Different effects were achieved by varying the proportions and concentrations of hydrophilic oil and PLGA. Scanning electron and optical microscopic images showed the surfaces of the microspheres to be smooth and that their morphology was spherical. Microspheres prepared using the w/o/oh/w emulsion were able to load protein efficiently and had sustained-release properties. These results indicate that the above-mentioned method might be useful for developing sustained-release microsphere formulations in the future. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Zyflamend suppresses growth and sensitizes human pancreatic tumors to gemcitabine in an orthotopic mouse model through modulation of multiple targets
Authors: Bokyung Sung
Jayaraj Ravindran
Sanjit Dey
Ajaikumar B Kunnumakkara
Juri G Gelovani
Sushovan Guha
Zhimin Tong
Bharat B Aggarwal
Amit Deorukhkar
Sunil Krishnan
Parmeswaran Diagaradjane
Cemile Koca
Journal: International Journal of Cancer (2012)
Discipline: CLINICAL MEDICINE
Keywords: pancreatic cancer; Zyflamend; gemcitabine; cell cultures; orthotopic mouse model
Affiliations: Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Abstract:  Agents that can potentiate the efficacy of standard chemotherapy against pancreatic cancer are of great interest. Because of their low cost and safety, patients commonly use a variety of dietary supplements, although evidence of their efficacy is often lacking. One such commonly used food supplement is Zyflamend, a polyherbal preparation with potent anti-inflammatory activities and preclinical efficacy against prostate and oral cancer. Whether Zyflamend has any efficacy against human pancreatic cancer alone or in combination with gemcitibine, a commonly used agent, was examined in cell cultures and in an orthotopic mouse model. In vitro, Zyflamend inhibited the proliferation of pancreatic cancer cell lines regardless of p53 status and also enhanced gemcitabine-induced apoptosis. This finding correlated with inhibition of NF-κB activation by Zyflamend and suppression of cyclin D1, c-myc, COX-2, Bcl-2, IAP, survivin, VEGF, ICAM-1 and CXCR4. In nude mice, oral administration of Zyflamend alone significantly inhibited the growth of orthotopically transplanted human pancreatic tumors, and when combined with gemcitabine, further enhanced the antitumor effects. Immunohistochemical and Western blot analyses of tumor tissue showed that the suppression of pancreatic cancer growth correlated with inhibition of proliferation index marker (Ki-67), COX-2, MMP-9, NF-κB and VEGF. Overall, these results suggest that the concentrated multiherb product Zyflamend alone can inhibit the growth of human pancreatic tumors and, in addition, can sensitize pancreatic cancers to gemcitabine through the suppression of multiple targets linked to tumorigenesis. 

Retracted: No

PubPeer comments:
 Figure 6C. * Blue boxes: Two panels appear to overlap. ![file] ,
Green synthesis of multifunctional silver and gold nanoparticles from the oriental herbal adaptogen: Siberian ginseng
Authors: Ramya Mathiyalagan
Yeon-Ju Kim
Priyanka Singh
Mohamed El-Agamy Farh
Josua Markus
Chao Wang
Ragavendran Abbai
Sungeun Ahn
Deok Chun Yang
Journal: International journal of nanomedicine (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Siberian ginseng; antibacterial activity; antioxidant efficacy; cytotoxicity; eleutheroside A
Affiliations: Ginseng Bank, Graduate School of Biotechnology.

Abstract:  Pharmacologically active stem of the oriental herbal adaptogen, Siberian ginseng, was employed for the ecofriendly synthesis of Siberian ginseng silver nanoparticles (Sg-AgNPs) and Siberian ginseng gold nanoparticles (Sg-AuNPs). First, for metabolic characterization of the sample, liquid chromatography-tandem mass spectrometry analysis (indicated the presence of eleutherosides A and E), total phenol content, and total reducing sugar were analyzed. Second, the water extract of the sample mediated the biological synthesis of both Sg-AgNPs and Sg-AuNPs that were crystalline face-centered cubical structures with a Z-average hydrodynamic diameter of 126 and 189 nm, respectively. Moreover, Fourier transform infrared analysis indicated that proteins and aromatic hydrocarbons play a key role in the formation and stabilization of Sg-AgNPs, whereas phenolic compounds accounted for the synthesis and stability of Sg-AuNPs. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H tetrazolium bromide (MTT) assay determined that Sg-AgNPs conferred strong cytotoxicity against MCF7 (human breast cancer cell line) and was only slightly toxic to HaCaT (human keratinocyte cell line) at 10 µg⋅mL(-1). However, Sg-AuNPs did not display cytotoxic effects against both of the cell lines. The disc diffusion assay indicated a dose-dependent increase in the zone of inhibition of Staphylococcus aureus (ATCC 6538), Bacillus anthracis (NCTC 10340), Vibrio parahaemolyticus (ATCC 33844), and Escherichia coli (BL21) treated with Sg-AgNPs, whereas Sg-AuNPs did not show inhibitory activity. In addition, the 2,2-diphenyl-1-picrylhydrazyl assay demonstrated that both Sg-AgNPs and Sg-AuNPs possess strong antioxidant activity. To the best of our knowledge, this is the first report unraveling the potential of Eleutherococcus senticosus for silver and gold nanoparticle synthesis along with its biological applications, which in turn would promote widespread usage of the endemic Siberian ginseng. 

Retracted: No

PubPeer comments:
 https: imgur.com a RwG8Pv9 ,
Spatial interplay between PIASy and FIP200 in the regulation of signal transduction and transcriptional activity
Authors: Klaus Schwamborn
Nadine Martin
Boyi Gan
Henning Urlaub
Anne Dejean
Jun-Lin Guan
Journal: Molecular and Cellular Biology (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PIAS family; transcriptional regulation; FIP200; protein interaction; SUMO
Affiliations: Nuclear Organization and Oncogenesis Unit, INSERM U579, Institut Pasteur, 75724 Paris Cedex 15, France., Nuclear Organization and Oncogenesis Unit, INSERM U579, Institut Pasteur, 75724 Paris Cedex 15, France, Bioanalytical Mass Spectrometry Group, Max Planck Institute for Biophysical Chemistry, D-37077 Goettingen, Germany, University of Michigan Medical School, Ann Arbor, Michigan 48109-2200

Abstract:  The members of the protein inhibitor of activated STAT (PIAS) family of proteins are implicated in fundamental cellular processes, including transcriptional regulation, either through action as E3 SUMO ligases or through SUMO-independent effects. We report here the identification of FIP200 (focal adhesion kinase family-interacting protein of 200 kDa) as a new PIASy-interacting protein. We show that the interaction depends on the integrity of the RING finger of PIASy and the carboxy terminus of FIP200. Both in vitro and in vivo sumoylation assays failed to reveal any sumoylation of FIP200, suggesting that FIP200 is not a bona fide SUMO substrate. Immunofluorescence microscopy and subcellular fractionation, either upon forced PIASy expression or in the absence of PIASy, revealed that interaction with PIASy redistributes FIP200 from the cytoplasm to the nucleus, correlating with abrogation of FIP200 regulation of TSC/S6K signaling. Conversely, FIP200 enhances the transcriptional activation of the p21 promoter by PIASy whereas PIASy transcription activity is severely reduced upon FIP200 depletion by RNA interference. Chromatin immunoprecipitation analysis demonstrates that endogenous PIASy and FIP200 are corecruited to the p21 promoter. Altogether, these results provide the first evidence for the existence of a close-spatially controlled-mode of regulation of FIP200 and PIASy nucleocytoplasmic functions. 

Retracted: No

PubPeer comments:
 ![file] , 
 Figure 3B. https: imgur.com ZYcVGON , 
 We thank PubPeer for bringing this issue to our attention. I am in contact with the co-authors to address this matter and will be back to PubPeer later. Sincerely, Anne Dejean , 
 Figure 2A. Vertical and horizontal straight edges. ![file] ,
Nanocrystallization of poorly water soluble drugs for parenteral administration
Authors: Bhuvaneshwer Vaidya
Amit K Goyal
Foziyah Zakir
S P Vyas
Karandeep Kaur
Himanshu Sharma
Basant Malik
Journal: Journal of biomedical nanotechnology (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: combinatorial chemistry; high-throughput screening; Nanoedge technology; Amphotericin B; surfactants
Affiliations: Rayat Institute of Pharmacy, Ropar, Punjab 144533, India.

Abstract:  Approximately 50% active substances discovered by combinatorial chemistry and high-throughput screening show poor solubility in water. Out of various available approaches "Nanoedege technology" (Combination of Precipitation and Homogenization) was selected. Amphotericin B (Amp B) was used as a model drug. Three different preparations of Amp B were produced by using three different surfactants Tween80, Pluronic F68, Soya Lecithin and assessed for their efficacy and stability. In this study the Amp B nanosuspension formulation, with the smaller particle size, can be effectively produced with the Nanoedge Method. The pharmacokinetic profiles of Amp B when given in the nanosuspension formulation were different compared to the corresponding raw drug. 

Retracted: No

PubPeer comments:
 Fig 2A:  the picture of Western blotting of IGF1R, RACK1, STAT3, Bcl-xl, Bcl-2 and Bax in the NPC and chronic nasopharyngitis tissues. ![file] These protein blobs appear over and over within an oeuvre, recorded in a spreadsheet: https: docs.google.com spreadsheets d 1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY edit?usp=sharing. They seem to come from the same restricted gamut shown in this montage: ![] , 
 Fig 1. Extensive overlaps. ![file] The existence of one corner where the yellow areas do **not** overlap creates concerns about the integrity of the images. , 
 Retracted [30 June 2021] . -------------------------- The above article, published online on 17 August 2017 in Wiley Online Library has been retracted by agreement between the the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. ,
Linifanib (ABT-869) Potentiates the Efficacy of Chemotherapeutic Agents through the Suppression of Receptor Tyrosine Kinase-Mediated AKT/mTOR Signaling Pathways in Gastric Cancer
Authors: Jing Chen
Jieqiong Wang
Jiawei Guo
Mingyao Liu
Zhi Chen
Xiufeng Pang
Journal: Scientific reports (2016)
Discipline: Multidisciplinary
Keywords: Gastric cancer; tumor angiogenesis; chemoresistance; linifanib; ABT-869
Affiliations: Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China., Key Laboratory of Reproduction and Genetics in Ningxia, Ningxia Medical University, Yinchuan 750004, China., Cancer Institute, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China., Institute of Biosciences and Technology, Department of Molecular and Cellular Medicine, Texas A&M University Health Science Center, Houston, Texas 77030, USA.

Abstract:  Gastric cancer, highly dependent on tumor angiogenesis, causes uncontrolled lethality, in part due to chemoresistance. Here, we demonstrate that linifanib (ABT-869), a novel multi-targeted receptor tyrosine kinase inhibitor, markedly augments cytotoxicity of chemotherapies in human gastric cancer. ABT-869 and chemotherapeutic agents exhibited a strong synergy to inhibit the viability of several gastric cancer cell lines, with combination index values ranging from 0.017 to 0.589. Additionally, the combination of ABT-869 and chemotherapeutic agents led to remarkable suppression of vascular endothelial growth factor (VEGF)-induced angiogenesis in vitro and in vivo. Importantly, in a preclinical gastric cancer xenograft mouse model, drug co-treatments led to increased mouse survival as well as a synergistic reduction in tumor size and the inhibition of tumor angiogenesis. Mechanistic studies further revealed that all of the co-treatments containing ABT-869 resulted in decreased activation of the VEGF receptor, the epidermal growth factor receptor and the insulin growth factor receptor. Inhibition of these receptor tyrosine kinases consequently attenuated the activation of the downstream AKT/mTOR signaling pathway both in cultured gastric cancer cells and in gastric cancer xenografts. Collectively, our findings suggest that the addition of ABT-869 to traditional chemotherapies may be a promising strategy for the treatment of human gastric cancer. 

Retracted: No

PubPeer comments:
 Figure 1a. Much more similar than expected. ![file] , 
 Figure 5. Much more similar than expected. ![file] , 
 Figure 5. Much more similar than expected. ![file] ,
MicroRNA-182 inhibits proliferation through targeting oncogenic ANUBL1 in gastric cancer
Authors: Feng Chen
Er-Jun Pang
Zhi-Qi Zhang
Wei-Feng Dong
Bing-Wei Jin
Lin Tang
Journal: Oncology Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNA-182; gastric cancer; ANUBL1; proliferation; colony formation
Affiliations: School of Basic Medical Sciences, Nanjing University of Chinese Medicine, Nanjing 210023, P.R. China., Division of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.

Abstract:  MicroRNA-182 (miR-182) is significantly downregulated in human gastric tissue samples. Overexpression of miR-182 suppresses the proliferation and colony formation of gastric cancer cells. However, new aspects of the mechanism are still emerging in gastric cancer. ANUBL1, also known as ZFAND4 (zinc finger, AN1-type domain 4), its roles are scarely reported in cancer. In this study, we not only showed that ANUBL1 as an oncogene was upregulated and could promote proliferation of SGC-7901 cells, but also demonstrated that its over-expression led to a strong decrease of miR-182 expression and expression of ANUBL1 was in turn directly downregulated by miR-182, thereby establishing a negative feedback loop between miR-182 and ANUBL1. The elucidation of the mechanisms of miR-182 targeting ANUBL1 in gastric cancer helps us to further understand the mechanism of gastric cancer initiation and progression. 

Retracted: No

PubPeer comments:
 Figure 2E and 4D: the merged images do not correspond with single stain images. ![file] , 
 Thank you for your commen.Contrast was adjusted separately for each image as it was produced. So there are subtle differences visible between a single photo and the Merge s photo. ,
Optoacoustic mesoscopy for biomedicine
Authors: Murad Omar
Vasilis Ntziachristos
Juan Aguirre
Journal: Nature Biomedical Engineering (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: optical microscopy; optoacoustic microscopy; optoacoustic mesoscopy; ultrasound detection; tissue pathophysiology
Affiliations: Institute of Biological and Medical Imaging, Helmholtz Zentrum München, Munich, Germany., Institute of Biological and Medical Imaging, Helmholtz Zentrum München, Munich, Germany. .

Abstract:  Fuelled by innovation, optical microscopy plays a critical role in the life sciences and medicine, from basic discovery to clinical diagnostics. However, optical microscopy is limited by typical penetration depths of a few hundred micrometres for in vivo interrogations in the visible spectrum. Optoacoustic microscopy complements optical microscopy by imaging the absorption of light, but it is similarly limited by penetration depth. In this Review, we summarize progress in the development and applicability of optoacoustic mesoscopy (OPAM); that is, optoacoustic imaging with acoustic resolution and wide-bandwidth ultrasound detection. OPAM extends the capabilities of optical imaging beyond the depths accessible to optical and optoacoustic microscopy, and thus enables new applications. We explain the operational principles of OPAM, its placement as a bridge between optoacoustic microscopy and optoacoustic macroscopy, and its performance in the label-free visualization of tissue pathophysiology, such as inflammation, oxygenation, vascularization and angiogenesis. We also review emerging applications of OPAM in clinical and biological imaging. 

Retracted: No

PubPeer comments:
 The authors describe optoacoustic photoacoustic imaging in their introduction as an  optical imaging method that is insensitive to photon scatter . This is a general misconception in the field since also diffuse illumination as it is used by acoustic resolution systems developed by the authors themselves is affected by scattering resulting in strong fluence decay over depth. A more adequate statement would be that the lateral resolution of acoustic resolution optoacoustics is not affected by photon scattering in regions where diffuse light propagation is still capable of providing enough light for sufficient SNR (typically only a few millimeters deep for optoacoustic mesoscopy RSOM). ,
LncRNA HCP5 promotes the development of cervical cancer by regulating MACC1 via suppression of microRNA-15a
Authors: D-M Fang
Q-J Meng
Y-H Xin
Y Yu
H-M Shen
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA HCP5; cervical cancer; MACC1; microRNA-15a; prognosis
Affiliations: Department of Reproductive, The Children and Women's Healthcare of Laiwu City, Laiwu, China. .

Abstract:  Objective: To explore the role of long non-coding RNA (lncRNA) HCP5 in the development of cervical cancer and its underlying mechanism. Patients and methods: Expression levels of HCP5, MACC1 and microRNA-15a in cervical cancer tissues and paracancerous tissues were detected. The relationship between HCP5 expression and prognosis of patients with cervical cancer was analyzed by Kaplan-Meier. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay after altering expressions of HCP5 and microRNA-15a by plasmids transfection. The binding condition of HCP5, MACC1 and microRNA-15a was evaluated by luciferase reporter gene assay. The regulatory effect of microRNA-15a on MACC1 expression was determined by Western blot. Results: HCP5 and MACC1 were overexpressed in cervical cancer tissues than those of paracancerous tissues. The survival rate of patients with cervical cancer was negatively correlated to HCP5 expression, but positively correlated to microRNA-15a expression. Luciferase reporter gene assay showed that microRNA-15a was directly bound to HCP5 and MACC1. Besides, overexpression of microRNA-15a could remarkably inhibited MACC1 expression. In vitro experiments showed that HCP5 promoted proliferation of cervical cancer cells, which was reversed by microRNA-15a knockdown. Conclusions: Overexpressed HCP5 promoted the development of cervical cancer through increasing MACC1 expression by microRNA-15a adsorption. 

Retracted: No

PubPeer comments:
 From the Methods:  *A total of 48 patients with cervical cancer who were treated in The First Peopleu2019s Hospital of Xianyang City during 2014 to 2016 were selected.* The paper was published in August 2018, four years after the first patients were selected, and two years after the last patients were enrolled. Yet, Figure 1D shows that the patients were followed for 5 years. Can the authors please explain how they did this? ![file] , 
 From the Methods:  *This study was approved by the Hospital Ethics Committee and patients signed the informed consent.* At which hospital was this Ethics Committee? The authors are from two different hospitals, so this statement is a bit vague. ,