Artículos de revista - Aldizkari artikuluak

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Open Access
Biochemistry, cytogenetics and DMD gene mutations in south indian patients with Duchenne muscular dystrophy
(Kamla-Raj Enterprises, 2017) Meyyazhagan, Arun; Raman, N. M.; Easwaran, M.; Balasubramanian, B.; Alagamuthu, K.; Kuchi Bhotla, H.; Shanmugam, S.; Inbaraj, K.; Ramesh Kumar, M.; Kumar, P.; Thangamani, L.; Piramanayagam, S.; Anand, V.; Mohd, Y.; Park, S.; Teijido Hermida, Óscar; Carril, Juan Carlos; Cacabelos, Pablo; Keshavarao, S.; Cacabelos, Ramón; Ciencias de la Salud; Osasun Zientziak
Thirty children aged 3-10 years with clinically confirmed or suspected Duchenne Muscular Dystrophy (DMD) were analyzed for chromosomal aberrations using cytological preparations, biochemical changes using enzyme kit protocol, and deletions in the 26 exons of the DMD gene by targeting the mutations at the proximal and distal ‘hot spot’ regions of the dystrophin gene in South Indian patients with DMD. The frequency of chromosomal aberrations (both chromosomal and chromatid-type) and serum enzyme levels were significantly elevated in DMD subjects as compared to controls. Multiplex PCR assays revealed 27 patients having deletions in the DMD gene located at the distal ‘hot spot’ region. This study suggests that disease progression is directly associated with higher incidence of the deletions at the distal ‘hot spot’ of the DMD gene.
Open Access
Population-based study of risk polymorphisms associated with vascular disorders and dementia
(Bentham Science Publishers, 2017) Teijido Hermida, Óscar; Carril, Juan Carlos ; Cacabelos, Ramón; Ciencias de la Salud; Osasun Zientziak
Introduction: Cardiovascular and neurodegenerative disorders are among the major causes of mortality in the developed countries. Population studies evaluate the genetic risk, i.e. the probability of an individual carrying a specific disease-associated polymorphism. Identification of risk polymorphisms is essential for an accurate diagnosis or prognosis of a number of pathologies. Aims: The aim of this study was to characterize the influence of risk polymorphisms associated with lipid metabolism, hypertension, thrombosis, and dementia, in a large population of Spanish individuals affected by a variety of brain and vascular disorders as well as metabolic syndrome. Material & Method: We performed a cross-sectional study on 4415 individuals from a widespread regional distribution in Spain (48.15% males and 51.85% females), with mental, neurodegenerative, cerebrovascular, and metabolic disorders. We evaluated polymorphisms in 20 genes involved in obesity, vascular and cardiovascular risk, and dementia in our population and compared it with representative Spanish and European populations. Risk polymorphisms in ACE, AGT(235), IL6(573), PSEN1, and APOE (specially the APOE-ε4 allele) are representative of our population as compared to the reference data of Spanish and European individuals. Conclusion: The significantly higher distribution of risk polymorphisms in PSEN1 and APOE-ε4 is characteristic of a representative number of patients with Alzheimer’s disease; whereas polymorphisms in ACE, AGT(235), and IL6(573), are most probably related with the high number of patients with metabolic syndrome or cerebrovascular damage.
Open Access
Pharmacogenetic considerations in the treatment of Alzheimer's disease
(Taylor & Francis, 2016) Cacabelos, Ramón; Torrellas, Clara; Teijido Hermida, Óscar; Carril, Juan Carlos ; Ciencias de la Salud; Osasun Zientziak
The practical pharmacogenetics of Alzheimer’s disease (AD) is circumscribed to acetylcholinesterase inhibitors (AChEIs) and memantine. However, pharmacogenetic procedures should be applied to novel strategies in AD therapeutics including: novel AChEIs and neurotransmitter regulators, anti-Aβ treatments, anti-tau treatments, pleiotropic products, epigenetic drugs and combination therapies. Genes involved in the pharmacogenetic network are under the influence of the epigenetic machinery which regulates gene expression transcriptionally and post-transcriptionally, configuring the fundamentals of pharmacoepigenomics. Over 60% of AD patients present concomitant pathologies demanding additional treatments which increase the likelihood of drug–drug interactions. Lipid metabolism dysfunction is a pathogenic mechanism inherent to AD neurodegeneration. The therapeutic response to hypolipidemic compounds is influenced by the APOE and CYP genotypes. The development of novel compounds and the use of combination/multifactorial treatments require the implantation of pharmacogenomic procedures for the avoidance of ADRs and the optimization of therapeutics.
Open Access
Epigenomics and proteomics of brain disorders
(SciTech Central, 2017-11-30) Cacabelos, Ramón; Meyyazhagan, Arun; Carril, Juan Carlos; Teijido Hermida, Óscar; Ciencias de la Salud; Osasun Zientziak
Epigenomic mechanisms (DNA methylation, chromatin remodeling/histone modifications, miRNA regulation) are involved in the transcriptional and post-translational regulation of genes in physiological and pathological conditions leading to potentially reversible phenotypes. Mutations in the genes encoding elements of the epigenetic machinery cause epigenetic Mendelian disorders. Epigenetic aberrations contribute to the pathogenesis of neurodevelopmental, imprinting, neuropsychiatric, and age-related neurodegenerative disorders. Some brain disorders exhibit proteoepigenomic changes resulting from primary genomic traits and/or secondary epigenetic events which induce pathogenic (structural, functional, conformational) changes in key proteins. Proteomic biomarkers and epigenomic signatures may help in the prediction, early diagnosis, and prognosis of CNS disorders. Epigenetic drug discovery, application of pharmacoepigenomic procedures for personalized therapeutics, novel approaches to decode and resolve drug resistance, and targeting miRNAs in prevention and treatment of brain disorders are promising areas of future development.
Open Access
Interrogating the epigenome to unveil the secrets of neurodegeneration: promising epigenetic therapies
(SciTech Central, 2016-07-25) Teijido Hermida, Óscar; Cacabelos, Ramón; Ciencias de la Salud; Osasun Zientziak
According to the WHO, cerebrovascular and neurodegenerative disorders affect one billion people around the world. Pathological phenotypes of neurodegeneration result from a combination of genomic, epigenomic, metabolic, and environmental factors, which hinder their treatment. Indeed, current FDA-approved conventional drugs used for treatment of neurodegenerative disorders provide very little beneficial effects, or, at best, reduce the pathological symptoms but do not detain disease progression. Furthermore, the unacceptable side effects of most of these treatments make them unsuitable for chronic treatments. One of the main reasons for this historical setback correlates with the poor knowledge about the molecular mechanisms of these pathologies, which results in the inappropriate drug target selection. Genetic components did not fully explain the mechanisms of those diseases. Furthermore, most treatments target symptomatic features of disease but they are not antipathogenic. During the last 15 years, the study of the role of the epigenetic machinery on gene regulation opens new and promising perspectives for a more accurate and effective treatment. Aberrant alterations in the epigenetic machinery result in dysregulation of gene expression at different levels in pathological conditions compared to healthy controls. The epigenetic approach allows the identification of key pathological targets in complex disorders that cannot be detected using genetic-based methods. Many of these epigenetic targets may be detected in early asymptomatic stages of the disease, which facilitates its treatment. Furthermore, the reversibility and potential restoring of epigenetic aberrations, unlike genetic mutations, sited epigenetic-based therapy as a promising tool to treat those complex disorders. This manuscript reviews the main epigenetic mechanisms involved in the most relevant neurodegenerative disorders nowadays, as well as the potential epigenetic-based drugs currently used in clinical trials for treatment of those disorders and future perspectives.
Open Access
Custodia compartida: maternidad intensiva y alterna
(Universidad Complutense de Madrid, 2025) Fernández Rasines, Paloma; Sociología y Trabajo Social; Soziologia eta Gizarte Lana
La custodia compartida es un modelo emergente de convivencia filioparental posdivorcio que se ha extendido en España de manera importante y progresiva, sobre todo en la última década. Este desarrollo ha tenido lugar en detrimento de la custodia exclusiva materna, que sigue siendo mayoritaria, a diferencia de la exclusiva paterna, que es muy excepcional. En este artículo ponemos el foco en visibilizar las prácticas maternales de mujeres que han decidido negociar acuerdos de corresponsabilidad parental con sus exparejas varones. La metodología utilizada incluye el análisis de los datos sobre custodia posruptura y un estudio empírico, realizado a partir de 2016, que incluye entrevistas focales a profesionales del servicio de mediación familiar extrajudicial del Gobierno de Navarra y entrevistas a mujeres madres, derivadas de este servicio público, como representantes de buenas prácticas de corresponsabilidad. Los resultados indican que este servicio constituye un instrumento de intervención y prevención para facilitar acuerdos sostenibles pero flexibles en el tiempo para el bienestar de los y las menores dependientes. Las mujeres entrevistadas son protagonistas en la toma de decisiones ante la ruptura y en la búsqueda de apoyo experto para la negociación. Al margen de este ejercicio de autonomía, se aprecia una prevalencia del género en la asignación de tiempos y calidad de crianza. La maternidad intensiva se atenúa con los acuerdos negociados tras el divorcio, pero la intendencia en las prácticas maternales se mantiene, aunque se realice de modo alterno o discontinuo. La reproducción estratificada explica desajustes a este mandato, como los que ilustran algunas prácticas maternales defectuosas que generan los condicionamientos de la política migratoria neocolonial.
Embargo
Enter Ftatateeta: name symbolism in Bernard Shaw's Caesar and Cleopatra
(Routledge, 2025-02-21) Rodríguez Martín, Gustavo A.; Goñi Alsúa, Edurne; Ciencias humanas y de la educación; Giza eta Hezkuntza Zientziak
This study explores the symbolism behind the name Ftatateeta, one of the characters in Bernard Shaw's Caesar and Cleopatra (1899). This character, one of Shaw's creations for the play, has a name that is both aurally salient and evocative of sartorial materials (i.e., tuftaffeta, taffeta). This symbolic name, in turn, goes hand in hand with the character's discourse and behaviour, as well as with her role as a stock character.
Open Access
La consideración de la innovación social en servicios sociales en las comunidades autónomas de España. Un estudio empírico de las tendencias actuales
(Universidades de Andalucía, 2024) Siria Mendaza, Sandra; Laparra Navarro, Miguel; Sociología y Trabajo Social; Soziologia eta Gizarte Lana
El concepto de innovación social puede aplicarse a numerosas áreas y es cada vez más habitual encontrarlo en el contexto de los servicios sociales. Se ha desarrollado una investigación descriptiva mediante análisis documental para identificar y analizar cuantitativa y cualitativamente una muestra de iniciativas de servicios sociales que han sido catalogadas como innovadoras por parte de agentes relevantes del sistema entre 2016 y 2022 en España. Los resultados permiten establecer una aproximación inicial sobre las líneas de actuación que se están considerando innovadoras en servicios sociales y valorar en qué medida están preconfigurando futuras transformaciones del conjunto del sistema.
Open Access
Pharmacogenomics of Alzheimer's disease: genetic determinants of phenotypic variation and therapeutic outcome
(SciTech Central, 2016-11-16) Cacabelos, Ramón; Carril, Juan Carlos; Cacabelos, Pablo; Teijido Hermida, Óscar; Goldgaber, Dmitry; Ciencias de la Salud; Osasun Zientziak
Alzheimer's disease is a polygenic/complex disorder in which genomic, epigenomic, cerebrovascular, metabolic, and environmental factors converge to define a progressive neurodegenerative phenotype. Conventional anti-dementia drugs are not cost-effective, and pharmacological breakthroughs have not been achieved for the past 10 years. Major determinants of therapeutic outcome in Alzheimer's disease (AD) include age- and sex-related factors, pathogenic phenotype, concomitant disorders, treatment modality and polypharmacy, and pharmacogenetics. Different categories of genes are potentially involved in the pharmacogenetic network responsible for drug efficacy and safety. Pathogenic, mechanistic, metabolic, transporter, and pleiotropic genes represent the major genetic determinants of response to treatment in AD. In pharmacogenetic studies, APOE-4 carriers are the worst responders and APOE-3 carriers are the best responders to conventional treatments. Patients harboring a large (L) number of poly T repeats in intrón 6 of the TOMM40 gene (L/L or S/L genotypes) in haplotypes associated with APOE-4 are the worst responders whereas patients with short (S) TOMM40 poly T variants (S/S genotype), and to a lesser extent S/VL and VL/VL carriers, in haplotypes with APOE-3 are the best responders to treatment. Only 25% of the Caucasian population are extensive metabolizers for trigenic haplotypes integrating CYP2D6- CYP2C19-CYP2C9 variants. Patients harboring CYP-related por (PM) and/or ultra-rapid (UM) geno-phenotypes display more irregular profiles in drug metabolism than extensive (EM) or intermediate (IM) metabolizers. Among 111 pentagenic (APOE-APOB-APOC3-CETP-LPL) haplotypes associated with lipid metabolism, carriers of the H26 haplotype (23-TT-CG- AG-CC) exhibit the lowest cholesterol levels and patients with the H104 haplotype (44-CC-CC-AA-CC) are severely hypercholesterolemic. Epigenetic aberrations (DNA methylation, histone modifications, miRNA dysregulation) in genes configuring the pharmacoepigenetic cascade also influence the response/resistance to drugs. Consequently, novel strategies in drug development, either preventive or therapeutic, for AD should take into consideration these pharmacogenetic determinants for treatment optimization.
Open Access
The reading rainbow of young multilingual learners: reading comprehension in the majority (Spanish), regional (Basque) and foreign (English) language
(Elsevier, 2025-03-31) Lázaro Ibarrola, Amparo; Luquin Urtasun, María; Roothooft, Hanne; Ciencias humanas y de la educación; Giza eta Hezkuntza Zientziak
Reading comprehension is crucial in education, serving as the foundation for acquiring knowledge. In multilingual settings, children must develop these skills in multiple languages. However, there is limited understanding of comprehension levels across languages and of the role of influencing factors such as language exposure, non-verbal intelligence (NVI), socioeconomic status (SES), and extramural reading (ER). This study explores how these variables impact the reading comprehension of young learners (aged 10–11) in English (foreign language), Spanish (main language), and Basque (regional language for Basque-immersion participants). The participants were divided into a high-intensity (HI) group (N = 118) and a low-intensity (LI) group (N = 81) within Basque-immersion programs. Results showed correlations among reading comprehension scores in Spanish, English, and Basque. While both groups demonstrated similar Spanish comprehension levels, the HI group excelled in English, particularly among high-NVI learners. LI learners scored lower in Basque compared to Spanish. Regression analyses indicated that NVI and, to a lesser extent, SES influenced reading comprehension across languages. Also, HI learners engaged more in English ER, whereas LI learners favored Basque. However, ER did not have a significant impact on their reading scores. Based on these findings, pedagogical implications for multilingual education contexts will be discussed.
Open Access
A lower affinity to cytosolic proteins reveals VDAC3 isoform-specific role in mitochondrial biology
(Rockefeller University Press, 2020-01-14) Queralt-Martín, María; Bergdoll, Lucie; Teijido Hermida, Óscar; Munshi, Nabill; Jacobs, Daniel; Kuszak, Adam J.; Protchenko, Olga; Reina, Simona; Magrì, Andrea; De Pinto, Vito; Bezrukov, Sergey M.; Abramson, Jeff; Rostovtseva, Tatiana K.; Ciencias de la Salud; Osasun Zientziak
Voltage-dependent anion channel (VDAC) is the major pathway for the transport of ions and metabolites across the mitochondrial outer membrane. Among the three known mammalian VDAC isoforms, VDAC3 is the least characterized, but unique functional roles have been proposed in cellular and animal models. Yet, a high-sequence similarity between VDAC1 and VDAC3 is indicative of a similar pore-forming structure. Here, we conclusively show that VDAC3 forms stable, highly conductive voltage-gated channels that, much like VDAC1, are weakly anion selective and facilitate metabolite exchange, but exhibit unique properties when interacting with the cytosolic proteins α-synuclein and tubulin. These two proteins are knowntobepotent regulators of VDAC1 andinduce similar characteristic blockages (on the millisecond time scale) of VDAC3, but with 10- to 100-fold reduced on-rates and altered α-synuclein blocking times, indicative of an isoform-specific function. Through cysteine scanning mutagenesis, we found that VDAC3’s cysteine residues regulate its interaction with α-synuclein, demonstrating VDAC3-unique functional properties and further highlighting a general molecular mechanism for VDAC isoform-specific regulation of mitochondrial bioenergetics.
Open Access
Magic angle spinning nuclear magnetic resonance characterization of voltage-dependent anion channel gating in two-dimensional lipid crystalline bilayers
(American Chemical Society, 2014-12-29) Eddy, Matthew T.; Andreas, Loren; Teijido Hermida, Óscar; Su, Yongchao; Clark, Lindsay; Noskov, Sergei Y.; Wagner, Gerhar; Rostovtseva, Tatiana K.; Griffin, Robert G.; Ciencias de la Salud; Osasun Zientziak
The N-terminus of the voltage-dependent anion channel (VDAC) has been proposed to contain the mechanistically important gating helices that modulate channel opening and closing. In this study, we utilize magic angle spinning nuclear magnetic resonance (MAS NMR) to determine the location and structure of the N-terminus for functional channels in lipid bilayers by measuring long-range 13C–13C distances between residues in the N-terminus and other domains of VDAC reconstituted into DMPC lipid bilayers. Our structural studies show that the distance between A14 Cβ in the N-terminal helix and S193 Cβ is ∼4–6 Å. Furthermore, VDAC phosphorylation by a mitochondrial kinase at residue S193 has been claimed to delay mitochondrial cell death by causing a conformational change that closes the channel, and a VDAC-Ser193Glu mutant has been reported to show properties very similar to those of phosphorylated VDAC in a cellular context. We expressed VDAC-S193E and reconstituted it into DMPC lipid bilayers. Two-dimensional 13C–13C correlation experiments showed chemical shift perturbations for residues located in the N-terminus, indicating possible structural perturbations to that region. However, electrophysiological data recorded on VDAC-S193E showed that channel characteristics were identical to those of wild type samples, indicating that phosphorylation of S193 does not directly affect channel gating. The combination of NMR and electrophysiological results allows us to discuss the validity of proposed gating models.
Open Access
MAC inhibitors antagonize the pro-apoptotic effects of tBid and disassemble Bax / Bak oligomer
(Springer, 2017) Peixoto, Pablo M.; Teijido Hermida, Óscar; Mirzalieva, Oygul; Dejean, Laurent M.; Pavlov, Evgeny V.; Antonsson, Bruno; Kinnally, Kathleen W.; Ciencias de la Salud; Osasun Zientziak
Open Access
A sandwich ELISA for the conformation-specific quantification of the activated form of human Bax
(Elsevier, 2016) Teijido Hermida, Óscar; Ganesan, Yogesh Tengarai; Llanos, Raul; Peton, Ashley; Urtecho, Jean-Baptiste; Soprani, Adauri; Villamayor, Aimee; Antonsson, Bruno; Manon, Stéphen; Dejean, Laurent M.; Ciencias de la Salud; Osasun Zientziak
Open Access
Bcl-xL stimulates Bax relocation to mitochondria and primes cells to ABT-737
(Elsevier, 2015) Renault, Thibaud T.; Teijido Hermida, Óscar; Missire, Florent; Ganesan, Yogesh Tengarai; Velours, Gisèle; Arokium, Hubert; Beaumatin, Florian; Llanos, Raul; Athané, Axel; Camougrand, Nadine; Priault, Muriel; Antonsson, Bruno; Dejean, Laurent M.; Manon, Stéphen; Ciencias de la Salud; Osasun Zientziak
Open Access
Conductance hysteresis in the voltage-dependent anion channel
(Springer, 2015) Rappaport, Shay M.; Teijido Hermida, Óscar; Hoogerheide, David P.; Rostovtseva, Tatiana K.; Berezhkovskii, Alexander M.; Bezrukov, Sergey M.; Ciencias de la Salud; Osasun Zientziak
Open Access
The weakness of common job contacts
(2023) Ruiz-Palazuelos, Sofía; Espinosa, María Paz; Kovarik, Jaromir; Economía; Ekonomia
This paper identifies an ignored driver of labor market outcomes in Calvó-Armengol (2004): the presence of overlapping neighborhoods in people’s social networks, a stylized fact of real world networks. We prove that short network cycles induce stochastic affiliation in diffusion processes channeled by networks, generating diffusion inefficiencies in the transmission of job information with persistent consequences on employment, wages, and inequality within and across networked societies. In particular, they organize employment probabilities in the sense of the first-order stochastic dominance: people in close-knit neighborhoods exhibit worse labor-market outcomes, even if they have the same number of information providers and compete with the same number of people for vacancies.Such a finding implies that the results in Calvó-Armengol (2004) are generally only valid for tree networks. Since dense, overlapping neighborhoods is one aspect of strong relationships, our findings uncover an alternative mechanism behind the strength of weak ties (Granovetter, 1973). Furthermore, short network cycles reinforce spatial and temporal correlations in employment status, shaping labor-market transition rates and amplifying aggregate employment fluctuations.
Open Access
Pharmacogenetics of vascular risk factors in Alzheimer's disease
(MDPI, 2018-01-03) Cacabelos, Ramón; Meyyazhagan, Arun; Carril, Juan Carlos; Cacabelos, Pablo; Teijido Hermida, Óscar; Ciencias de la Salud; Osasun Zientziak
Alzheimer's disease (AD) is a polygenic/complex disorder in which genomic, epigenomic, cerebrovascular, metabolic, and environmental factors converge to define a progressive neurodegenerative phenotype. Pharmacogenetics is a major determinant of therapeutic outcome in AD. Different categories of genes are potentially involved in the pharmacogenetic network responsible for drug efficacy and safety, including pathogenic, mechanistic, metabolic, transporter, and pleiotropic genes. However, most drugs exert pleiotropic effects that are promiscuously regulated for different gene products. Only 20% of the Caucasian population are extensive metabolizers for tetragenic haplotypes integrating CYP2D6-CYP2C19-CYP2C9-CYP3A4/5 variants. Patients harboring CYP-related poor (PM) and/or ultra-rapid (UM) geno-phenotypes display more irregular profiles in drug metabolism than extensive (EM) or intermediate (IM) metabolizers. Among 111 pentagenic (APOE-APOB-APOC3-CETP-LPL) haplotypes associated with lipid metabolism, carriers of the H26 haplotype (23-TT-CG-AG-CC) exhibit the lowest cholesterol levels, and patients with the H104 haplotype (44-CC-CC-AA-CC) are severely hypercholesterolemic. Furthermore, APOE, NOS3, ACE, AGT, and CYP variants influence the therapeutic response to hypotensive drugs in AD patients with hypertension. Consequently, the implementation of pharmacogenetic procedures may optimize therapeutics in AD patients under polypharmacy regimes for the treatment of concomitant vascular disorders.
Open Access
Pharmacoepigenomic interventions as novel potential treatments for Alzheimer's and Parkinson's diseases
(MDPI, 2018) Teijido Hermida, Óscar; Cacabelos, Ramón; Ciencias de la Salud; Osasun Zientziak
Cerebrovascular and neurodegenerative disorders affect one billion people around the world and result from a combination of genomic, epigenomic, metabolic, and environmental factors. Diagnosis at late stages of disease progression, limited knowledge of gene biomarkers and molecular mechanisms of the pathology, and conventional compounds based on symptomatic rather than mechanistic features, determine the lack of success of current treatments, including current FDA-approved conventional drugs. The epigenetic approach opens new avenues for the detection of early presymptomatic pathological events that would allow the implementation of novel strategies in order to stop or delay the pathological process. The reversibility and potential restoring of epigenetic aberrations along with their potential use as targets for pharmacological and dietary interventions sited the use of epidrugs as potential novel candidates for successful treatments of multifactorial disorders involving neurodegeneration. This manuscript includes a description of the most relevant epigenetic mechanisms involved in the most prevalent neurodegenerative disorders worldwide, as well as the main potential epigenetic-based compounds under investigation for treatment of those disorders and their limitations.
Embargo
Compensation strategy to minimize over-cut effects in robotic belt grinding with passive-compliant tools
(Elsevier, 2025-03-19) Torres Izu, Ramón; Iriarte Goñi, Xabier; Mata Cantón, Sara; Aginaga García, Jokin; Barrenetxea Azpeitia, David; Ingeniería; Ingeniaritza; Institute of Smart Cities - ISC; Gobierno de Navarra / Nafarroako Gobernua
At the beginning of the robotic belt grinding path, passive-compliant tools can generate an over-cut effect. The transient state from the first contact point between tool and workpiece to the grinding steady state can generate an excess of material removal at the workpiece border. If successive grinding passes are made, this effect will accumulate, increasing the shape deviation at the workpiece border. Therefore, the purpose of this research is to analyze this phenomenon and develop an easy-to-implement compensation strategy to avoid removing an excess of material at the beginning of grinding paths. Specifically, a geometric model of the contact has been developed that, together with the material removal model, allows to reproduce the cut-in effect for a robot-operated passive-compliant tool case. In turn, the compensation strategy that has been designed, avoids removing an excessive amount of material by means of a cut-in path that adjusts the feed velocity to the instantaneous contact force. This path is based on the tool geometry and grinding process parameters. In order to validate the proposed strategy, several experiments have been performed for different process conditions. Results show how the proposed solution significantly reduces the over-cut effect providing a homogeneous material removal since the beginning of the grinding.