113 research outputs found
Plan de Contingencia. Acción A2 “Planificación técnica de las acciones de restauración”
El marco de trabajo creado al amparo del proyecto LIFE FLUVIAL “Mejora y
gestión sostenible de los corredores fluviales de la Región Atlántica Ibérica”
(LIFE16 NAT/ES/000771), contempla la puesta en marcha una estrategia
transnacional para la gestión sostenible de sus hábitats en varias cuencas fluviales
atlánticas de la Península Ibérica (España y Portugal).
El objetivo general del proyecto es la mejora del estado de conservación de
corredores fluviales atlánticos en la Red Natura 2000. En este ámbito, factores de
amenaza como especies invasoras, intensificación de usos o problemas
fitosanitarios, generan el deterioro y fragmentación de los hábitats de los
corredores fluviales. Estas amenazas inciden sobre la calidad y continuidad de los
bosques higrófilos, hábitat principal al que va dirigido el proyecto, considerado de
carácter prioritario (91E0* Bosques aluviales con Alnus glutinosa y Fraxinus
excelsior) y pieza clave en el mantenimiento de la composición, estructura y
funcionalidad de los corredores fluviales. El proyecto aporta estrategias de gestión
transnacional que permitan mitigar y corregir los efectos negativos de las
amenazas identificadas, así como evitar su expansión hacia otros territorios de la
UE. El proyecto considera otro hábitat objetivo: 9230 Robledales galaico-
portugueses con Quercus robur y Quercus pyrenaica, que representa la continuidad
con el tipo de hábitat 91E0*.
Para alcanzar el objetivo general se plantean objetivos específicos
encaminados a combatir la degradación de los hábitats:
1. Desarrollo de un modelo transnacional de gestión sostenible de
corredores fluviales para la mejora de su estado de conservación, mediante la
restauración de la composición, estructura y funcionalidad de sus tipos de hábitats,
la mejora de la conectividad y la reducción de la fragmentación
2. Control de flora exótica e invasora
3. Mejora del estado fitosanitario de los corredores fluviales, mediante
la retirada parcial de árboles muertos
4. Difusión y sensibilización de los valores naturales, beneficios
socioeconómicos y servicios ecosistémicos prestados por los corredores fluviales
5. Mejora de la formación y capacitación técnica de los agentes
implicados en la gestión y conservación de los corredores fluviales
La consecución de los objetivos del proyecto se realizará mediante la
ejecución de 8 acciones concretas de conservación en 9 espacios Natura 2000 de
España y Portugal. Para su puesta en marcha, el proyecto plantea la elaboración de
una serie de documentos de planificación técnica en los que se recojan las
soluciones adoptadas y la metodología a ser puesta en marcha. No obstante, ante
posibles riesgos e imprevistos que puedan surgir al implementar las acciones de
conservación, se hace necesaria la disposición de un plan de contingencia, que
permita establecer las soluciones necesarias para llevar adelante la actuación.info:eu-repo/semantics/publishedVersio
Abstracts
Tradução, para a língua inglesa, dos resumos dos artigos publicados nesta edição
Contribution of TEX15 genetic variants to the risk of developing severe non-obstructive oligozoospermia
Background: Severe spermatogenic failure (SPGF) represents one of the most relevant causes of male infertility. This pathological condition can lead to extreme abnormalities in the seminal sperm count, such as severe oligozoospermia (SO) or non-obstructive azoospermia (NOA). Most cases of SPGF have an unknown aetiology, and it is known that this idiopathic form of male infertility represents a complex condition. In this study, we aimed to evaluate whether common genetic variation in TEX15, which encodes a key player in spermatogenesis, is involved in the susceptibility to idiopathic SPGF.Materials and Methods: We designed a genetic association study comprising a total of 727 SPGF cases (including 527 NOA and 200 SO) and 1,058 unaffected men from the Iberian Peninsula. Following a tagging strategy, three tag single-nucleotide polymorphisms (SNPs) of TEX15 (rs1362912, rs323342, and rs323346) were selected for genotyping using TaqMan probes. Case-control association tests were then performed by logistic regression models. In silico analyses were also carried out to shed light into the putative functional implications of the studied variants.Results: A significant increase in TEX15-rs1362912 minor allele frequency (MAF) was observed in the group of SO patients (MAF = 0.0842) compared to either the control cohort (MAF = 0.0468, OR = 1.90, p = 7.47E-03) or the NOA group (MAF = 0.0472, OR = 1.83, p = 1.23E-02). The genotype distribution of the SO population was also different from those of both control (p = 1.14E-02) and NOA groups (p = 4.33-02). The analysis of functional annotations of the human genome suggested that the effect of the SO-associated TEX15 variants is likely exerted by alteration of the binding affinity of crucial transcription factors for spermatogenesis.Conclusion: Our results suggest that common variation in TEX15 is involved in the genetic predisposition to SO, thus supporting the notion of idiopathic SPGF as a complex trait
Contribution of TEX15 genetic variants to the risk of developing severe non-obstructive oligozoospermia
Lisbon clinical group co-authors and
IVIRMA group co-authors
Ana Aguiar, (Unidade de Medicina da Reproducao,
Hospital de Santa Maria, Centro Hospitalar Lisboa Norte,
Lisboa, Portugal); Carlos Calhaz-Jorge, (Unidade de Medicina
da Reproducao, Hospital de Santa Maria, Centro Hospitalar
Lisboa Norte, Lisboa, Portugal); Joaquim Nunes, (Unidade de
Medicina da Reproducao, Hospital de Santa Maria, Centro
Hospitalar Lisboa Norte, Lisboa, Portugal); Sandra Sousa
(Unidade de Medicina da Reproducao, Hospital de Santa
Maria, Centro Hospitalar Lisboa Norte, Lisboa, Portugal),
and Sónia Correia (Centro de Medicina Reprodutiva,
Maternidade Alfredo da Costa, Centro Hospitalar Lisboa
Central, Lisboa, Portugal); Maria Graça Pinto(Centro de
Medicina Reprodutiva, Maternidade Alfredo da Costa,
Centro Hospitalar Lisboa Central, Lisboa, Portugal).
Alberto Pacheco, (IVIRMA Madrid, Spain); Cristina
González, (IVIRMA Sevilla, Spain); Susana Gómez,
(IVIRMA Lisboa, Portugal); David Amorós, (IVIRMA
Barcelona, Spain); Jesús Aguilar, (IVIRMA Vigo, Spain);
Fernando Quintana, (IVIRMA Bilbao, Spain).Background: Severe spermatogenic failure (SPGF) represents one of the most relevant causes of male infertility. This pathological condition can lead to extreme abnormalities in the seminal sperm count, such as severe oligozoospermia (SO) or non-obstructive azoospermia (NOA). Most cases of SPGF have an unknown aetiology, and it is known that this idiopathic form of male infertility represents a complex condition. In this study, we aimed to evaluate whether common genetic variation in TEX15, which encodes a key player in spermatogenesis, is involved in the susceptibility to idiopathic SPGF.
Materials and Methods: We designed a genetic association study comprising a total of 727 SPGF cases (including 527 NOA and 200 SO) and 1,058 unaffected men from the Iberian Peninsula. Following a tagging strategy, three tag single-nucleotide polymorphisms (SNPs) of TEX15 (rs1362912, rs323342, and rs323346) were selected for genotyping using TaqMan probes. Case-control association tests were then performed by logistic regression models. In silico analyses were also carried out to shed light into the putative functional implications of the studied variants.
Results: A significant increase in TEX15-rs1362912 minor allele frequency (MAF) was observed in the group of SO patients (MAF = 0.0842) compared to either the control cohort (MAF = 0.0468, OR = 1.90, p = 7.47E-03) or the NOA group (MAF = 0.0472, OR = 1.83, p = 1.23E-02). The genotype distribution of the SO population was also different from those of both control (p = 1.14E-02) and NOA groups (p = 4.33–02). The analysis of functional annotations of the human genome suggested that the effect of the SO-associated TEX15 variants is likely exerted by alteration of the binding affinity of crucial transcription factors for spermatogenesis.
Conclusion: Our results suggest that common variation in TEX15 is involved in the genetic predisposition to SO, thus supporting the notion of idiopathic SPGF as a complex trait.This work was supported by the Spanish Ministry of
Science and Innovation through the Spanish National Plan
for Scientific and Technical Research and Innovation (PID
2020-120157RB-I00) and the Andalusian Government
through the research projects of “Plan Andaluz de
Investigacion, Desarrollo e Innovacion (PAIDI 2020)” (ref.
PY20_00212) and “Programa Operativo FEDER 2020” (ref.
B-CTS-584-UGR20). LB-C was supported by the Spanish
Ministry of Science and Innovation through the “Juan de la
Cierva Incorporacion” program (Grant ref. IJC 2018-038026-
I, funded by MCIN/AEI/10.13039/501100011033), which
includes FEDER funds. AG-J was funded by MCIN/AEI/
10.13039/501100011033 and FSE “El FSE invierte en tu
futuro” (grant ref. FPU20/02926). IPATIMUP integrates
the i3S Research Unit, which is partially supported by the
Portuguese Foundation for Science and Technology (FCT),
financed by the European Social Funds (COMPETE-FEDER)
and National Funds (projects PEstC/SAU/LA0003/2013 and
POCI-01-0145-FEDER-007274). PM is supported by the FCT
post-doctoral fellowship (SFRH/BPD/120777/2016), financed
from the Portuguese State Budget of the Ministry for Science, Technology and High Education and from the European
Social Fund, available through the Programa Operacional
do Capital Humano. ToxOmics—Centre for
Toxicogenomics and Human Health, Genetics, Oncology
and Human Toxicology, Nova Medical School, Lisbon, is
also partially supported by FCT (UID/BIM/00009/2016 and
UIDB/00009/2020). SL received support from Instituto de
Salud Carlos III (grant: DTS18/00101], co-funded by
FEDER funds/European Regional Development Fund
(ERDF)-a way to build Europe-), and from “Generalitat de
Catalunya” (grant 2017SGR191). SL is sponsored by the
“Researchers Consolidation Program” from the SNS-Dpt.
Salut Generalitat de Catalunya (Exp. CES09/020). This
article is related to the Ph.D. Doctoral Thesis of AG-J.info:eu-repo/semantics/publishedVersio
Common genetic variation in KATNAL1 non-coding regions is involved in the susceptibility to severe phenotypes of male infertility
Free PMC article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9546047/Background: Previous studies in animal models evidenced that genetic mutations
of KATNAL1, resulting in dysfunction of its encoded protein, lead to male infertility
through disruption of microtubule remodelling and premature germ cell exfoliation.
Subsequent studies in humans also suggested a possible role of KATNAL1 single nucleotide polymorphisms in the development of male infertility as a consequence of
severe spermatogenic failure.
Objectives: The main objective of the present study is to evaluate the effect of the
common genetic variation of KATNAL1 in a large and phenotypically well-characterised
cohort of infertile men because of severe spermatogenic failure.
Materials and methods: A total of 715 infertile men because of severe spermato genic failure, including 210 severe oligospermia and 505 non-obstructive azoospermia
patients, as well as 1058 unaffected controls were genotyped for three KATNAL1
single-nucleotide polymorphism taggers (rs2077011, rs7338931 and rs2149971).
Case–control association analyses by logistic regression assuming different models
and in silico functional characterisation of risk variants were conducted.
Results: Genetic associations were observed between the three analysed taggers and
different severe spermatogenic failure groups. However, in all cases, the haplotype
model (rs2077011*C | rs7338931*T | rs2149971*A) better explained the observed
associations than the three risk alleles independently. This haplotype was associated
with non-obstructive azoospermia (adjusted p = 4.96E-02, odds ratio = 2.97), Sertoli cell only syndrome (adjusted p = 2.83E-02, odds ratio = 5.16) and testicular sperm
extraction unsuccessful outcomes (adjusted p = 8.99E-04, odds ratio = 6.13). The in
silico analyses indicated that the effect on severe spermatogenic failure predisposition
could be because of an alteration of the KATNAL1 splicing pattern.
Conclusions: Specific allelic combinations of KATNAL1 genetic polymorphisms may
confer a risk of developing severe male infertility phenotypes by favouring the
overrepresentation of a short non-functional transcript isoform in the testis.This work was supported by the Spanish Ministry of Economy and
Competitiveness through the Spanish National Plan for Scientific
and Technical Research and Innovation (refs. SAF2016-78722-R and
PID2020-120157RB-I00), the ‘Instituto de Salud Carlos III’ (Fondo
de Investigaciones Sanitarias)/Fondo Europeo de Desarrollo Regional
‘Una manera de hacer Europa’ (FIS/FEDER) (ref. DTS18/00101 to
Sara Larriba), the Generalitat de Catalunya (ref. 2017SGR191), the
‘Ramón y Cajal’ program (ref. RYC-2014-16458) and the ‘Juan de
la Cierva Incorporación’ program (ref. IJC2018-038026-I), as well as
the Andalusian Government through the R&D&i Projects Grants for
Universities and Public Research Entities (ref. PY20_00212), which
include FEDER funds. Andrea Guzmán-Jiménez was a recipient of a
grant from the Spanish Ministry of Education and Professional Training (‘Becas de Colaboración en Departamentos Universitarios para el curso académico 2020/2021’). Patricia I. Marques is supported by
the FCT post-doctoral fellowship (SFRH/BPD/120777/2016), financed
from the Portuguese State Budget of the Ministry for Science, Tech nology and High Education and from the European Social Fund,
available through the ‘Programa Operacional do Capital Humano’. João
Gonçalves was partially funded by FCT/MCTES through national funds
attributed to the Centre for Toxicogenomics and Human Health—
ToxOmics (UID/BIM/00009/2016 and UIDB/00009/2020). Sara Larriba is sponsored by the Researchers Consolidation Program (ISCIII
SNS/Dpt. Salut Generalitat de Catalunya) (CES09/020).info:eu-repo/semantics/publishedVersio
Common genetic variation in KATNAL1 non‐coding regions is involved in the susceptibility to severe phenotypes of male infertility
© 2022 The Authors. Andrology published by Wiley Periodicals LLC on behalf of American Society of Andrology and European Academy of Andrology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.Background: Previous studies in animal models evidenced that genetic mutations of KATNAL1, resulting in dysfunction of its encoded protein, lead to male infertility through disruption of microtubule remodelling and premature germ cell exfoliation. Subsequent studies in humans also suggested a possible role of KATNAL1 single-nucleotide polymorphisms in the development of male infertility as a consequence of severe spermatogenic failure.
Objectives: The main objective of the present study is to evaluate the effect of the common genetic variation of KATNAL1 in a large and phenotypically well-characterised cohort of infertile men because of severe spermatogenic failure.
Materials and methods: A total of 715 infertile men because of severe spermatogenic failure, including 210 severe oligospermia and 505 non-obstructive azoospermia patients, as well as 1058 unaffected controls were genotyped for three KATNAL1 single-nucleotide polymorphism taggers (rs2077011, rs7338931 and rs2149971). Case-control association analyses by logistic regression assuming different models and in silico functional characterisation of risk variants were conducted.
Results: Genetic associations were observed between the three analysed taggers and different severe spermatogenic failure groups. However, in all cases, the haplotype model (rs2077011*C | rs7338931*T | rs2149971*A) better explained the observed associations than the three risk alleles independently. This haplotype was associated with non-obstructive azoospermia (adjusted p = 4.96E-02, odds ratio = 2.97), Sertoli-cell only syndrome (adjusted p = 2.83E-02, odds ratio = 5.16) and testicular sperm extraction unsuccessful outcomes (adjusted p = 8.99E-04, odds ratio = 6.13). The in silico analyses indicated that the effect on severe spermatogenic failure predisposition could be because of an alteration of the KATNAL1 splicing pattern.
Conclusions: Specific allelic combinations of KATNAL1 genetic polymorphisms may confer a risk of developing severe male infertility phenotypes by favouring the overrepresentation of a short non-functional transcript isoform in the testis.This work was supported by the Spanish Ministry of Economy and Competitiveness through the Spanish National Plan for Scientific and Technical Research and Innovation (refs. SAF2016-78722-R and PID2020-120157RB-I00), the ‘Instituto de Salud Carlos III’ (Fondo de Investigaciones Sanitarias)/Fondo Europeo de Desarrollo Regional ‘Una manera de hacer Europa’ (FIS/FEDER) (ref. DTS18/00101 to Sara Larriba), the Generalitat de Catalunya (ref. 2017SGR191), the ‘Ramón y Cajal’ program (ref. RYC-2014-16458) and the ‘Juan de la Cierva Incorporación’ program (ref. IJC2018-038026-I), as well as the Andalusian Government through the R&D&i Projects Grants for Universities and Public Research Entities (ref. PY20_00212), which include FEDER funds. Andrea Guzmán-Jiménez was a recipient of a grant from the Spanish Ministry of Education and Professional Training (‘Becas de Colaboración en Departamentos Universitarios para el curso académico 2020/2021’). Patricia I. Marques is supported by the FCT post-doctoral fellowship (SFRH/BPD/120777/2016), financed from the Portuguese State Budget of the Ministry for Science, Technology and High Education and from the European Social Fund, available through the ‘Programa Operacional do Capital Humano’. João Gonçalves was partially funded by FCT/MCTES through national funds attributed to the Centre for Toxicogenomics and Human Health—ToxOmics (UID/BIM/00009/2016 and UIDB/00009/2020). Sara Larriba is sponsored by the Researchers Consolidation Program (ISCIII SNS/Dpt. Salut Generalitat de Catalunya) (CES09/020).info:eu-repo/semantics/publishedVersio
Common Variation in the PIN1 Locus Increases the Genetic Risk to Suffer from Sertoli Cell-Only Syndrome
Funding Information: Funding: This work was supported by the Plan Andaluz de Investigación, Desarrollo e Innovación (PAIDI 2020) (ref. PY20_00212, P20_00583), and the Spanish Ministry of Economy and Competitiveness through the Spanish National Plan for Scientific and Technical Research and Innovation (ref. SAF2016–78722-R, PID2020–120157RB-I00) and the Proyectos I + D + i del Programa Operativo FEDER 2020 (ref. B-CTS-584-UGR20, B-CTS-260-UGR20). FDC was supported by the “Ramón y Cajal” program (ref. RYC-2014–16458), and LBC was supported by the Spanish Ministry of Economy and Competitiveness through the “Juan de la Cierva Incorporación” program (Grant ref. IJC2018– 038026-I, funded by MCIN/AEI/10.13039/501100011033), all of them including FEDER funds. AGJ was funded by MCIN/AEI/10.13039/501100011033 and FSE “El FSE invierte en tu futuro”(grant ref. FPU20/02926). SGM was funded by a previously mentioned project (ref. PY20_00212). IPATIMUP integrates the i3S Research Unit, which is partially supported by the Portuguese Foundation for Science and Technology (FCT), financed by the European Social Funds (COMPETE-FEDER) and National Funds (projects PEstC/SAU/LA0003/2013 and POCI-01–0145-FEDER-007274). AML is funded by the Portuguese Government through FCT (IF/01262/2014). PIM is supported by the FCT post-doctoral fellowship (SFRH/BPD/120777/2016), financed from the Portuguese State Budget of the Ministry for Science, Technology and High Education and from the European Social Fund, available through the Programa Operacional do Capital Humano. ToxOmics—Centre for Toxicogenomics and Human Health, Genetics, Oncology and Human Toxicology, Nova Medical School, Lisbon, is also partially supported by FCT (Projects: UID/BIM/00009/2013 and UIDB/UIDP/00009/2020). SLarriba received support from Instituto de Salud Carlos III (grant DTS18/00101], co-funded by FEDER funds/European Regional Development Fund (ERDF)—a way to build Europe), and from “Generalitat de Catalunya” (grant 2017SGR191). SLarriba is sponsored by the “Researchers Consolidation Program” from the SNS-Dpt. Salut Generalitat de Catalunya (Exp. CES09/020). This article is related to the Ph.D. Doctoral Thesis of Miriam Cerván-Martín (grant ref. BES-2017–081222 funded by MCIN/AEI/10.13039/501100011033 and FSE “El FSE invierte en tu futuro”). Publisher Copyright: © 2022 by the authors. Licensee MDPI, Basel, Switzerland.We aimed to analyze the role of the common genetic variants located in the PIN1 locus, a relevant prolyl isomerase required to control the proliferation of spermatogonial stem cells and the integrity of the blood–testis barrier, in the genetic risk of developing male infertility due to a severe spermatogenic failure (SPGF). Genotyping was performed using TaqMan genotyping assays for three PIN1 taggers (rs2287839, rs2233678 and rs62105751). The study cohort included 715 males diagnosed with SPGF and classified as suffering from non-obstructive azoospermia (NOA, n = 505) or severe oligospermia (SO, n = 210), and 1058 controls from the Iberian Peninsula. The allelic frequency differences between cases and controls were analyzed by the means of logistic regression models. A subtype specific genetic association with the subset of NOA patients classified as suffering from the Sertoli cell-only (SCO) syndrome was observed with the minor alleles showing strong risk effects for this subset (ORaddrs2287839 = 1.85 (1.17–2.93), ORaddrs2233678 = 1.62 (1.11–2.36), ORaddrs62105751 = 1.43 (1.06–1.93)). The causal variants were predicted to affect the binding of key transcription factors and to produce an altered PIN1 gene expression and isoform balance. In conclusion, common non-coding single-nucleotide polymorphisms located in PIN1 increase the genetic risk to develop SCO.publishersversionpublishe
Immune and spermatogenesis-related loci are involved in the development of extreme patterns of male infertility
We conducted a genome-wide association study in a large population of infertile men due to unexplained spermatogenic failure (SPGF). More than seven million genetic variants were analysed in 1,274 SPGF cases and 1,951 unaffected controls from two independent European cohorts. Two genomic regions were associated with the most severe histological pattern of SPGF, defined by Sertoli cell-only (SCO) phenotype, namely the MHC class II gene HLA-DRB1 (rs1136759, P = 1.32E-08, OR = 1.80) and an upstream locus of VRK1 (rs115054029, P = 4.24E-08, OR = 3.14), which encodes a protein kinase involved in the regulation of spermatogenesis. The SCO-associated rs1136759 allele (G) determines a serine in the position 13 of the HLA-DR beta 1 molecule located in the antigen-binding pocket. Overall, our data support the notion of unexplained SPGF as a complex trait influenced by common variation in the genome, with the SCO phenotype likely representing an immune-mediated condition. A GWAS in a large case-control cohort of European ancestry identifies two genomic regions, the MHC class II gene HLA-DRB1 and an upstream locus of VRK1, that are associated with the most severe phenotype of spermatogenic failure
Treatment with tocilizumab or corticosteroids for COVID-19 patients with hyperinflammatory state: a multicentre cohort study (SAM-COVID-19)
Objectives: The objective of this study was to estimate the association between tocilizumab or corticosteroids and the risk of intubation or death in patients with coronavirus disease 19 (COVID-19) with a hyperinflammatory state according to clinical and laboratory parameters.
Methods: A cohort study was performed in 60 Spanish hospitals including 778 patients with COVID-19 and clinical and laboratory data indicative of a hyperinflammatory state. Treatment was mainly with tocilizumab, an intermediate-high dose of corticosteroids (IHDC), a pulse dose of corticosteroids (PDC), combination therapy, or no treatment. Primary outcome was intubation or death; follow-up was 21 days. Propensity score-adjusted estimations using Cox regression (logistic regression if needed) were calculated. Propensity scores were used as confounders, matching variables and for the inverse probability of treatment weights (IPTWs).
Results: In all, 88, 117, 78 and 151 patients treated with tocilizumab, IHDC, PDC, and combination therapy, respectively, were compared with 344 untreated patients. The primary endpoint occurred in 10 (11.4%), 27 (23.1%), 12 (15.4%), 40 (25.6%) and 69 (21.1%), respectively. The IPTW-based hazard ratios (odds ratio for combination therapy) for the primary endpoint were 0.32 (95%CI 0.22-0.47; p < 0.001) for tocilizumab, 0.82 (0.71-1.30; p 0.82) for IHDC, 0.61 (0.43-0.86; p 0.006) for PDC, and 1.17 (0.86-1.58; p 0.30) for combination therapy. Other applications of the propensity score provided similar results, but were not significant for PDC. Tocilizumab was also associated with lower hazard of death alone in IPTW analysis (0.07; 0.02-0.17; p < 0.001).
Conclusions: Tocilizumab might be useful in COVID-19 patients with a hyperinflammatory state and should be prioritized for randomized trials in this situatio
Sloan Digital Sky Survey IV: mapping the Milky Way, nearby galaxies, and the distant universe
We describe the Sloan Digital Sky Survey IV (SDSS-IV), a project encompassing three major spectroscopic programs. The Apache Point Observatory Galactic Evolution Experiment 2 (APOGEE-2) is observing hundreds of thousands of Milky Way stars at high resolution and high signal-to-noise ratios in the near-infrared. The Mapping Nearby Galaxies at Apache Point Observatory (MaNGA) survey is obtaining spatially resolved spectroscopy for thousands of nearby galaxies (median ). The extended Baryon Oscillation Spectroscopic Survey (eBOSS) is mapping the galaxy, quasar, and neutral gas distributions between and 3.5 to constrain cosmology using baryon acoustic oscillations, redshift space distortions, and the shape of the power spectrum. Within eBOSS, we are conducting two major subprograms: the SPectroscopic IDentification of eROSITA Sources (SPIDERS), investigating X-ray AGNs and galaxies in X-ray clusters, and the Time Domain Spectroscopic Survey (TDSS), obtaining spectra of variable sources. All programs use the 2.5 m Sloan Foundation Telescope at the Apache Point Observatory; observations there began in Summer 2014. APOGEE-2 also operates a second near-infrared spectrograph at the 2.5 m du Pont Telescope at Las Campanas Observatory, with observations beginning in early 2017. Observations at both facilities are scheduled to continue through 2020. In keeping with previous SDSS policy, SDSS-IV provides regularly scheduled public data releases; the first one, Data Release 13, was made available in 2016 July
- …