michi-zuri/pubmed-fatalTitle-set.txt

## pubmed-fatalTitle-set.txt
PMID- 32026671
OWN - NLM
STAT- Publisher
LR  - 20200206
IS  - 1001-0939 (Print)
IS  - 1001-0939 (Linking)
VI  - 43
IP  - 0
DP  - 2020 Feb 6
TI  - [Analysis of clinical features of 29 patients with 2019 novel coronavirus
      pneumonia].
PG  - E005
LID - 10.3760/cma.j.issn.1001-0939.2020.0005 [doi]
AB  - Objective: To analyze the clinical characteristics of 2019 novel coronavirus
      (2019-nCoV) pneumonia and to investigate the correlation between serum inflammatory
      cytokines and severity of the disease. Methods: 29 patients with 2019-ncov admitted
      to the isolation ward of Tongji hospital affiliated to Tongji medical college of
      Huazhong University of Science and Technology in January 2020 were selected as the
      study subjects. Clinical data were collected and the general information, clinical
      symptoms, blood test and CT imaging characteristics were analyzed. According to the
      relevant diagnostic criteria, the patients were divided into three groups: mild (15
      cases), severe (9 cases) and critical (5 cases). The expression levels of
      inflammatory cytokines and other markers in the serum of each group were detected,
      and the changes of these indicators of the three groups were compared and analyzed,
      as well as their relationship with the clinical classification of the disease.
      Results: (1) The main symptoms of 2019-nCoV pneumonia was fever (28/29) with or
      without respiratory and other systemic symptoms. Two patients died with underlying
      disease and co-bacterial infection, respectively. (2) The blood test of the patients
      showed normal or decreased white blood cell count (23/29), decreased lymphocyte
      count (20/29), increased hypersensitive C reactive protein (hs-CRP) (27/29), and
      normal procalcitonin. In most patients,serum lactate dehydrogenase (LDH) was
      significantly increased (20/29), while albumin was decreased(15/29). Alanine
      aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (Tbil),
      serum creatinine (Scr) and other items showed no significant changes. (3) CT
      findings of typical cases were single or multiple patchy ground glass shadows
      accompanied by septal thickening. When the disease progresses, the lesion increases
      and the scope expands, and the ground glass shadow coexists with the solid shadow or
      the stripe shadow. (4) There were statistically significant differences in the
      expression levels of interleukin-2 receptor (IL-2R) and IL-6 in the serum of the
      three groups (P<0.05), among which the critical group was higher than the severe
      group and the severe group was higher than the mildgroup. However, there were no
      statistically significant differences in serum levels of tumor necrosis factor-alpha
      (TNF-α), IL-1, IL-8, IL-10, hs-CRP, lymphocyte count and LDH among the three groups
      (P>0.05). Conclusion: The clinical characteristics of 2019-nCoV pneumonia are
      similar to those of common viral pneumonia. High resolution CT is of great value in
      the differential diagnosis of this disease. The increased expression of IL-2R and
      IL-6 in serum is expected to predict the severity of the 2019-nCoV pneumonia and the
      prognosis of patients.
FAU - Chen, L
AU  - Chen L
AD  - Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji
      Medical College Huazhong University of Science and Technology, Wuhan430030, China.
FAU - Liu, H G
AU  - Liu HG
AD  - Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji
      Medical College Huazhong University of Science and Technology, Wuhan430030, China.
FAU - Liu, W
AU  - Liu W
AD  - Department of Respiratory and Critical Care Medicine, the Central Hospital of Wuhan,
      Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014,
      China.
FAU - Liu, J
AU  - Liu J
AD  - Department of Radiology, Wuhan Pulmonary Hospital, Tongji Medical College, Huazhong
      University of Science and Technology, Wuhan 430030, China.
FAU - Liu, K
AU  - Liu K
AD  - Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji
      Medical College Huazhong University of Science and Technology, Wuhan430030, China.
FAU - Shang, J
AU  - Shang J
AD  - Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji
      Medical College Huazhong University of Science and Technology, Wuhan430030, China.
FAU - Deng, Y
AU  - Deng Y
AD  - Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji
      Medical College Huazhong University of Science and Technology, Wuhan430030, China.
FAU - Wei, S
AU  - Wei S
AD  - Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji
      Medical College Huazhong University of Science and Technology, Wuhan430030, China.
LA  - chi
PT  - English Abstract
PT  - Journal Article
DEP - 20200206
PL  - China
TA  - Zhonghua Jie He He Hu Xi Za Zhi
JT  - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of
      tuberculosis and respiratory diseases
JID - 8712226
SB  - IM
OTO - NOTNLM
OT  - 2019 novel coronavirus pneumonia
OT  - Clinical features
OT  - Disease severity
OT  - Inflammatory cytokines
EDAT- 2020/02/07 06:00
MHDA- 2020/02/07 06:00
CRDT- 2020/02/07 06:00
PHST- 2020/02/07 06:00 [entrez]
PHST- 2020/02/07 06:00 [pubmed]
PHST- 2020/02/07 06:00 [medline]
AID - 10.3760/cma.j.issn.1001-0939.2020.0005 [doi]
PST - aheadofprint
SO  - Zhonghua Jie He He Hu Xi Za Zhi. 2020 Feb 6;43(0):E005. doi:
      10.3760/cma.j.issn.1001-0939.2020.0005.

PMID- 31306780
OWN - NLM
STAT- In-Process
LR  - 20200715
IS  - 1523-6536 (Electronic)
IS  - 1083-8791 (Print)
IS  - 1083-8791 (Linking)
VI  - 25
IP  - 11
DP  - 2019 Nov
TI  - Outcomes of Hematopoietic Cell Transplantation in Patients with Germline
      SAMD9/SAMD9L Mutations.
PG  - 2186-2196
LID - S1083-8791(19)30439-2 [pii]
LID - 10.1016/j.bbmt.2019.07.007 [doi]
AB  - Germline mutations in SAMD9 and SAMD9L genes cause MIRAGE (myelodysplasia,
      infection, restriction of growth, adrenal hypoplasia, genital phenotypes, and
      enteropathy) (OMIM: *610456) and ataxia-pancytopenia (OMIM: *611170) syndromes,
      respectively, and are associated with chromosome 7 deletions, myelodysplastic
      syndrome (MDS), and bone marrow failure. In this retrospective series, we report
      outcomes of allogeneic hematopoietic cell transplantation (HCT) in patients with
      hematologic disorders associated with SAMD9/SAMD9L mutations. Twelve patients
      underwent allogeneic HCT for MDS (n = 10), congenital amegakaryocytic
      thrombocytopenia (n = 1), and dyskeratosis congenita (n = 1). Exome sequencing
      revealed heterozygous mutations in SAMD9 (n = 6) or SAMD9L (n = 6) genes. Four SAMD9
      patients had features of MIRAGE syndrome. Median age at HCT was 2.8 years (range,
      1.2 to 12.8 years). Conditioning was myeloablative in 9 cases and reduced intensity
      in 3 cases. Syndrome-related comorbidities (diarrhea, infections, adrenal
      insufficiency, malnutrition, and electrolyte imbalance) were present in MIRAGE
      syndrome cases. One patient with a familial SAMD9L mutation, MDS, and morbid obesity
      failed to engraft and died of refractory acute myeloid leukemia. The other 11
      patients achieved neutrophil engraftment. Acute post-transplant course was
      complicated by syndrome-related comorbidities in MIRAGE cases. A patient with
      SAMD9L-associated MDS died of diffuse alveolar hemorrhage. The other 10 patients had
      resolution of hematologic disorder and sustained peripheral blood donor chimerism.
      Ten of 12 patients were alive with a median follow-up of 3.1 years (range, 0.1 to
      14.7 years). More data are needed to refine transplant approaches in SAMD9/SAMD9L
      patients with significant comorbidities and to develop guidelines for their
      long-term follow-up.
CI  - Copyright © 2019 American Society for Transplantation and Cellular Therapy.
      Published by Elsevier Inc. All rights reserved.
FAU - Ahmed, Ibrahim A
AU  - Ahmed IA
AD  - Division of Pediatric Hematology, Oncology and Blood and Marrow Transplantation,
      Department of Pediatrics, Children's Mercy Kansas City, Kansas City, Missouri.
FAU - Farooqi, Midhat S
AU  - Farooqi MS
AD  - Department of Pathology and Laboratory Medicine, Children's Mercy Kansas City,
      Kansas City, Missouri.
FAU - Vander Lugt, Mark T
AU  - Vander Lugt MT
AD  - Division of Pediatric Hematology/Oncology, Department of Pediatrics, C. S. Mott
      Children's Hospital, University of Michigan, Ann Arbor, Michigan.
FAU - Boklan, Jessica
AU  - Boklan J
AD  - Department of Oncology, Phoenix Children's Hospital, Phoenix, Arizona.
FAU - Rose, Melissa
AU  - Rose M
AD  - Hematology & Oncology, Nationwide Children's Hospital, Columbus, Ohio.
FAU - Friehling, Erika D
AU  - Friehling ED
AD  - Division of Pediatric Hematology/Oncology, Department of Pediatrics, UPMC Children's
      Hospital of Pittsburgh, Pittsburgh, Pennsylvania.
FAU - Triplett, Brandon
AU  - Triplett B
AD  - Department of Bone Marrow Transplant, St. Jude Children's Research Hospital,
      Memphis, Tennessee.
FAU - Lieuw, Kenneth
AU  - Lieuw K
AD  - Department of Pediatrics, Walter Reed National Military Medical Center, Bethesda,
      Maryland.
FAU - Saldana, Blachy Davila
AU  - Saldana BD
AD  - Division of Blood and Marrow Transplantation, Children's National Medical Center,
      Washington, DC.
FAU - Smith, Christine M
AU  - Smith CM
AD  - Division of Hematology-Oncology, Department of Pediatrics, Vanderbilt University
      Medical Center, Nashville, Tennessee.
FAU - Schwartz, Jason R
AU  - Schwartz JR
AD  - Hematology Department, St. Jude Children's Research Hospital, Memphis, Tennessee.
FAU - Goyal, Rakesh K
AU  - Goyal RK
AD  - Division of Pediatric Hematology, Oncology and Blood and Marrow Transplantation,
      Department of Pediatrics, Children's Mercy Kansas City, Kansas City, Missouri.
      Electronic address: rkgoyal@cmh.edu.
LA  - eng
PT  - Journal Article
DEP - 20190712
TA  - Biol Blood Marrow Transplant
JT  - Biology of blood and marrow transplantation : journal of the American Society for
      Blood and Marrow Transplantation
JID - 9600628
SB  - IM
PMC - PMC7110513
OTO - NOTNLM
OT  - *Germline
OT  - *Inherited bone marrow failure syndromes
OT  - *MIRAGE syndrome
OT  - *Monosomy 7
OT  - *Myelodysplastic syndrome
OT  - *SAMD9/SAMD9 mutations
EDAT- 2019/07/16 06:00
MHDA- 2019/07/16 06:00
CRDT- 2019/07/16 06:00
PHST- 2019/03/17 00:00 [received]
PHST- 2019/06/14 00:00 [revised]
PHST- 2019/07/05 00:00 [accepted]
PHST- 2019/07/16 06:00 [pubmed]
PHST- 2019/07/16 06:00 [medline]
PHST- 2019/07/16 06:00 [entrez]
AID - S1083-8791(19)30439-2 [pii]
AID - 10.1016/j.bbmt.2019.07.007 [doi]
PST - ppublish
SO  - Biol Blood Marrow Transplant. 2019 Nov;25(11):2186-2196. doi:
      10.1016/j.bbmt.2019.07.007. Epub 2019 Jul 12.

PMID- 31835559
OWN - NLM
STAT- In-Process
LR  - 20200602
IS  - 1999-4915 (Electronic)
IS  - 1999-4915 (Linking)
VI  - 11
IP  - 12
DP  - 2019 Dec 10
TI  - Feline Infectious Peritonitis as a Systemic Inflammatory Disease: Contribution of
      Liver and Heart to the Pathogenesis.
LID - 10.3390/v11121144 [doi]
LID - 1144
AB  - Feline infectious peritonitis (FIP) is a fatal immune-mediated disease of cats,
      induced by feline coronavirus (FCoV). A combination of as yet poorly understood host
      and viral factors combine to cause a minority of FCoV-infected cats to develop FIP.
      Clinicopathological features include fever, vasculitis, and serositis, with or
      without effusions; all of which indicate a pro-inflammatory state with cytokine
      release. As a result, primary immune organs, as well as circulating leukocytes, have
      thus far been of most interest in previous studies to determine the likely sources
      of these cytokines. Results have suggested that these tissues alone may not be
      sufficient to induce the observed inflammation. The current study therefore focussed
      on the liver and heart, organs with a demonstrated ability to produce cytokines and
      therefore with huge potential to exacerbate inflammatory processes. The IL-12:IL-10
      ratio, a marker of the immune system's inflammatory balance, was skewed towards the
      pro-inflammatory IL-12 in the liver of cats with FIP. Both organs were found to
      upregulate mRNA expression of the inflammatory triad of cytokines IL-1β, IL-6, and
      TNF-α in FIP. This amplifying step may be one of the missing links in the
      pathogenesis of this enigmatic disease.
FAU - Malbon, Alexandra J
AU  - Malbon AJ
AD  - Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, 8057
      Zurich, Switzerland.
AD  - Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, 8057 Zurich,
      Switzerland.
FAU - Fonfara, Sonja
AU  - Fonfara S
AD  - Department of Clinical Studies, Ontario Veterinary College, University of Guelph,
      Guelph, ON N1G 2W1, Canada.
AD  - Small Animal Hospital, Faculty of Veterinary Medicine, University of Helsinki, 00014
      Helsinki, Finland.
AD  - Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, University
      of Helsinki, 00014 Helsinki, Finland.
FAU - Meli, Marina L
AU  - Meli ML
AUID- ORCID: 0000-0002-3609-2416
AD  - Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, 8057 Zurich,
      Switzerland.
AD  - Clinical Laboratory, Vetsuisse Faculty, University of Zurich, 8057 Zurich,
      Switzerland.
FAU - Hahn, Shelley
AU  - Hahn S
AD  - Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, University
      of Helsinki, 00014 Helsinki, Finland.
FAU - Egberink, Herman
AU  - Egberink H
AUID- ORCID: 0000-0001-6852-5936
AD  - Virology Division, Department of Infectious Diseases and Immunology, Faculty of
      Veterinary Medicine, Utrecht University, 3584 CL Utrecht, The Netherlands.
FAU - Kipar, Anja
AU  - Kipar A
AD  - Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, 8057
      Zurich, Switzerland.
AD  - Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, 8057 Zurich,
      Switzerland.
AD  - Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, University
      of Helsinki, 00014 Helsinki, Finland.
LA  - eng
GR  - WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191210
TA  - Viruses
JT  - Viruses
JID - 101509722
SB  - IM
PMC - PMC6949997
OTO - NOTNLM
OT  - *cardiomyocytes
OT  - *feline coronavirus
OT  - *feline infectious peritonitis
OT  - *hepatocytes
OT  - *inflammatory cytokines
OT  - *pathogenesis
OT  - *systemic inflammatory response
COIS- The authors declare no conflict of interest.
EDAT- 2019/12/15 06:00
MHDA- 2019/12/15 06:00
CRDT- 2019/12/15 06:00
PHST- 2019/10/31 00:00 [received]
PHST- 2019/12/06 00:00 [revised]
PHST- 2019/12/06 00:00 [accepted]
PHST- 2019/12/15 06:00 [entrez]
PHST- 2019/12/15 06:00 [pubmed]
PHST- 2019/12/15 06:00 [medline]
AID - v11121144 [pii]
AID - viruses-11-01144 [pii]
AID - 10.3390/v11121144 [doi]
PST - epublish
SO  - Viruses. 2019 Dec 10;11(12):1144. doi: 10.3390/v11121144.

PMID- 31214181
OWN - NLM
STAT- In-Process
LR  - 20200413
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 10
DP  - 2019
TI  - Environmental and Molecular Drivers of the α-Gal Syndrome.
PG  - 1210
LID - 10.3389/fimmu.2019.01210 [doi]
LID - 1210
AB  - The α-Gal syndrome (AGS) is a type of allergy characterized by an IgE antibody (Ab)
      response against the carbohydrate Galα1-3Galβ1-4GlcNAc-R (α-Gal), which is present
      in glycoproteins from tick saliva and tissues of non-catarrhine mammals. Recurrent
      tick bites induce high levels of anti-α-Gal IgE Abs that mediate delayed
      hypersensitivity to consumed red meat products in humans. This was the first
      evidence that tick glycoproteins play a major role in allergy development with the
      potential to cause fatal delayed anaphylaxis to α-Gal-containing foods and drugs and
      immediate anaphylaxis to tick bites. Initially, it was thought that the origin of
      tick-derived α-Gal was either residual blood meal mammalian glycoproteins containing
      α-Gal or tick gut bacteria producing this glycan. However, recently tick
      galactosyltransferases were shown to be involved in α-Gal synthesis with a role in
      tick and tick-borne pathogen life cycles. The tick-borne pathogen Anaplasma
      phagocytophilum increases the level of tick α-Gal, which potentially increases the
      risk of developing AGS after a bite by a pathogen-infected tick. Two mechanisms
      might explain the production of anti-α-Gal IgE Abs after tick bites. The first
      mechanism proposes that the α-Gal antigen on tick salivary proteins is presented to
      antigen-presenting cells and B-lymphocytes in the context of Th(2) cell-mediated
      immunity induced by tick saliva. The second mechanism is based on the possibility
      that tick salivary prostaglandin E2 triggers Immunoglobulin class switching to
      anti-α-Gal IgE-producing B cells from preexisting mature B cells clones producing
      anti-α-Gal IgM and/or IgG. Importantly, blood group antigens influence the capacity
      of the immune system to produce anti-α-Gal Abs which in turn impacts individual
      susceptibility to AGS. The presence of blood type B reduces the capacity of the
      immune system to produce anti-α-Gal Abs, presumably due to tolerance to α-Gal, which
      is very similar in structure to blood group B antigen. Therefore, individuals with
      blood group B and reduced levels of anti-α-Gal Abs have lower risk to develop AGS.
      Specific immunity to tick α-Gal is linked to host immunity to tick bites. Basophil
      activation and release of histamine have been implicated in IgE-mediated acquired
      protective immunity to tick infestations and chronic itch. Basophil reactivity was
      also found to be higher in patients with AGS when compared to asymptomatic α-Gal
      sensitized individuals. In addition, host resistance to tick infestation is
      associated with resistance to tick-borne pathogen infection. Anti-α-Gal IgM and IgG
      Abs protect humans against vector-borne pathogens and blood group B individuals seem
      to be more susceptible to vector-borne diseases. The link between blood groups and
      anti-α-Gal immunity which in turn affects resistance to vector-borne pathogens and
      susceptibility to AGS, suggests a trade-off between susceptibility to AGS and
      protection to some infectious diseases. The understanding of the environmental and
      molecular drivers of the immune mechanisms involved in AGS is essential to
      developing tools for the diagnosis, control, and prevention of this growing health
      problem.
FAU - Cabezas-Cruz, Alejandro
AU  - Cabezas-Cruz A
AD  - UMR BIPAR, INRA, ANSES, Ecole Nationale Vétérinaire d'Alfort, Université Paris-Est,
      Maisons-Alfort, France.
FAU - Hodžić, Adnan
AU  - Hodžić A
AD  - Department of Pathobiology, Institute of Parasitology, University of Veterinary
      Medicine Vienna, Vienna, Austria.
FAU - Román-Carrasco, Patricia
AU  - Román-Carrasco P
AD  - Molecular Biotechnology Section, University of Applied Sciences, Vienna, Austria.
FAU - Mateos-Hernández, Lourdes
AU  - Mateos-Hernández L
AD  - UMR BIPAR, INRA, ANSES, Ecole Nationale Vétérinaire d'Alfort, Université Paris-Est,
      Maisons-Alfort, France.
FAU - Duscher, Georg Gerhard
AU  - Duscher GG
AD  - Department of Pathobiology, Institute of Parasitology, University of Veterinary
      Medicine Vienna, Vienna, Austria.
FAU - Sinha, Deepak Kumar
AU  - Sinha DK
AD  - Biology Center, Institute of Parasitology, Czech Academy of Sciences, Ceské
      Budějovice, Czechia.
FAU - Hemmer, Wolfgang
AU  - Hemmer W
AD  - FAZ-Floridsdorf Allergy Center, Vienna, Austria.
FAU - Swoboda, Ines
AU  - Swoboda I
AD  - Molecular Biotechnology Section, University of Applied Sciences, Vienna, Austria.
FAU - Estrada-Peña, Agustín
AU  - Estrada-Peña A
AD  - Faculty of Veterinary Medicine, University of Zaragoza, Zaragoza, Spain.
FAU - de la Fuente, José
AU  - de la Fuente J
AD  - SaBio, Instituto de Investigación de Recursos Cinegéticos, IREC-CSIC-UCLM-JCCM,
      Ciudad Real, Spain.
AD  - Department of Veterinary Pathobiology, Center for Veterinary Health Sciences,
      Oklahoma State University, Stillwater, OK, United States.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20190531
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
SB  - IM
PMC - PMC6554561
OTO - NOTNLM
OT  - *IgE
OT  - *food allergy
OT  - *red meat allergy
OT  - *ticks
OT  - *α-Gal syndrome (AGS)
EDAT- 2019/06/20 06:00
MHDA- 2019/06/20 06:00
CRDT- 2019/06/20 06:00
PHST- 2019/03/14 00:00 [received]
PHST- 2019/05/13 00:00 [accepted]
PHST- 2019/06/20 06:00 [entrez]
PHST- 2019/06/20 06:00 [pubmed]
PHST- 2019/06/20 06:00 [medline]
AID - 10.3389/fimmu.2019.01210 [doi]
PST - epublish
SO  - Front Immunol. 2019 May 31;10:1210. doi: 10.3389/fimmu.2019.01210. eCollection 2019.

PMID- 31139181
OWN - NLM
STAT- In-Process
LR  - 20200414
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 10
DP  - 2019
TI  - The IL-12 Cytokine and Receptor Family in Graft-vs.-Host Disease.
PG  - 988
LID - 10.3389/fimmu.2019.00988 [doi]
LID - 988
AB  - Allogeneic hematopoietic cell transplantation (allo-HCT) is performed with curative
      intent for high- risk blood cancers and bone marrow failure syndromes; yet the
      development of acute and chronic graft-vs.-host disease (GVHD) remain preeminent
      causes of death and morbidity. The IL-12 family of cytokines is comprised of IL-12,
      IL-23, IL-27, IL-35, and IL-39. This family of cytokines is biologically distinct in
      that they are composed of functional heterodimers, which bind to cognate
      heterodimeric receptor chains expressed on T cells. Of these, IL-12 and IL-23 share
      a common β cytokine subunit, p40, as well as a receptor chain: IL-12Rβ1. IL-12 and
      IL-23 have been documented as proinflammatory mediators of GVHD, responsible for T
      helper 1 (Th1) differentiation and T helper 17 (Th17) stabilization, respectively.
      The role of IL-27 is less defined, seemingly immune suppressive via IL-10 secretion
      by Type 1 regulatory (Tr1) cells yet promoting inflammation through impairing CD4(+)
      T regulatory (Treg) development and/or enhancing Th1 differentiation. More recently,
      IL-35 was described as a potent anti-inflammatory agent produced by regulatory B and
      T cells. The role of the newest member, IL-39, has been implicated in
      proinflammatory B cell responses but has not been explored in the context of
      allo-HCT. This review is directed at discussing the current literature relevant to
      each IL-12-family cytokine and cognate receptor engagement, as well as the
      consequential downstream signaling implications, during GVHD pathogenesis.
      Additionally, we will provide an overview of translational strategies targeting the
      IL-12 family cytokines, their receptors, and subsequent signal transduction to
      control GVHD.
FAU - Bastian, David
AU  - Bastian D
AD  - Department of Microbiology and Immunology, Medical University of South Carolina,
      Charleston, SC, United States.
FAU - Wu, Yongxia
AU  - Wu Y
AD  - Department of Microbiology and Immunology, Medical University of South Carolina,
      Charleston, SC, United States.
FAU - Betts, Brian C
AU  - Betts BC
AD  - Department of Medicine, University of Minnesota, Minneapolis, MN, United States.
FAU - Yu, Xue-Zhong
AU  - Yu XZ
AD  - Department of Microbiology and Immunology, Medical University of South Carolina,
      Charleston, SC, United States.
AD  - Department of Medicine, Medical University of South Carolina, Charleston, SC, United
      States.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190508
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
SB  - IM
PMC - PMC6518430
OTO - NOTNLM
OT  - *GVHD
OT  - *GVT
OT  - *HCT
OT  - *IL-12 cytokines
OT  - *IL-12 family cytokine receptors
OT  - *cytokine
OT  - *cytokine receptor
OT  - *signal transduction
EDAT- 2019/05/30 06:00
MHDA- 2019/05/30 06:00
CRDT- 2019/05/30 06:00
PHST- 2019/01/09 00:00 [received]
PHST- 2019/04/16 00:00 [accepted]
PHST- 2019/05/30 06:00 [entrez]
PHST- 2019/05/30 06:00 [pubmed]
PHST- 2019/05/30 06:00 [medline]
AID - 10.3389/fimmu.2019.00988 [doi]
PST - epublish
SO  - Front Immunol. 2019 May 8;10:988. doi: 10.3389/fimmu.2019.00988. eCollection 2019.

PMID- 30878710
OWN - NLM
STAT- In-Process
LR  - 20200506
IS  - 2213-2201 (Electronic)
VI  - 7
IP  - 6
DP  - 2019 Jul-Aug
TI  - Spectrum of Pulmonary Aspergillosis in Hyper-IgE Syndrome with Autosomal-Dominant
      STAT3 Deficiency.
PG  - 1986-1995.e3
LID - S2213-2198(19)30263-6 [pii]
LID - 10.1016/j.jaip.2019.02.041 [doi]
AB  - BACKGROUND: Autosomal-dominant signal transducer and activator of transcription 3
      (STAT3) deficiency predisposes to recurrent bacterial pneumonia, complicated by
      bronchiectasis and cavitations. Aspergillosis is a major cause of morbidity in these
      patients. However, its diagnosis, classification, and treatment are challenging.
      OBJECTIVE: We aimed to assess the prevalence and describe the clinical, mycological,
      and radiological presentation and related therapy and outcome of Aspergillus
      infections of the respiratory tract in the STAT3-deficient patients of the National
      French cohort. METHODS: We performed a retrospective study of all pulmonary
      aspergillosis cases in STAT3-deficient patients (n = 74). Clinical and mycological
      data were collected up to October 2015 and imaging was centralized. RESULTS:
      Twenty-one episodes of pulmonary aspergillosis in 13 (17.5%) STAT3-deficient
      patients were identified. The median age at first episode was 13 years
      (interquartile range, 10-26 years). Ninety percent of patients had previous
      bronchiectasis or cavitations. Infections were classified as follows: 5 single
      aspergilloma, 9 chronic cavity pulmonary aspergillosis, 5 allergic bronchopulmonary
      aspergillosis-like disease, and 2 mixed forms of concomitant allergic
      bronchopulmonary aspergillosis-like disease and chronic cavity pulmonary
      aspergillosis. No invasive aspergillosis cases were identified. Aspergillus species
      were isolated in 71% of episodes and anti-Aspergillus antibodies in 93%. Eleven
      episodes were breakthrough infections. Antifungal treatment was prolonged, with a
      median of 13 months, and 6 patients (7 episodes) required surgery, with a high rate
      of postsurgical complications. One patient died and 6 had a relapse. CONCLUSIONS:
      Chronic and allergic forms of aspergillosis occurred in 17.5% of STAT3-deficient
      patients, mostly in lung cavities. Almost half had recurrences, despite prolonged
      antifungal treatment and/or surgery.
CI  - Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by
      Elsevier Inc. All rights reserved.
FAU - Duréault, Amélie
AU  - Duréault A
AD  - Service de Maladies Infectieuses et Tropicales, Hôpital Necker-Enfants Malades,
      Assistance Publique-Hôpitaux de Paris (APHP), Université Paris Descartes, Paris,
      France.
FAU - Tcherakian, Colas
AU  - Tcherakian C
AD  - Service de Pneumologie, Hôpital Foch, Suresnes, France; Faculté des Sciences de la
      Santé Simone Veil, Université Versailles-Saint-Quentin-en-Yvelines, Versailles,
      France; National Referral Center for Hypereosinophilic (CEREO).
FAU - Poiree, Sylvain
AU  - Poiree S
AD  - Service de Radiologie, Hôpital Necker-Enfants Malades, APHP, Paris, France.
FAU - Catherinot, Emilie
AU  - Catherinot E
AD  - Service de Pneumologie, Hôpital Foch, Suresnes, France; Faculté des Sciences de la
      Santé Simone Veil, Université Versailles-Saint-Quentin-en-Yvelines, Versailles,
      France.
FAU - Danion, François
AU  - Danion F
AD  - Service de Maladies Infectieuses et Tropicales, Hôpital Necker-Enfants Malades,
      Assistance Publique-Hôpitaux de Paris (APHP), Université Paris Descartes, Paris,
      France.
FAU - Jouvion, Grégory
AU  - Jouvion G
AD  - Unité de Neuropathologie Expérimentale, Institut Pasteur, Paris, France; Département
      de Génétique Médicale, Hôpital Trousseau, Sorbonne Université, APHP, Paris, France.
FAU - Bougnoux, Marie Elisabeth
AU  - Bougnoux ME
AD  - Service de Microbiologie, Hôpital Necker-Enfants Malades, APHP, Paris, France.
FAU - Mahlaoui, Nizar
AU  - Mahlaoui N
AD  - Centre d'Etude des Déficits Immunitaires (CEDI), Hôpital Necker-Enfants Malades,
      APHP, Paris, France; CEREDIH, Centre de Référence des Déficits Immunitaires
      Héréditaires, Hôpital Universitaire Necker-Enfants Malades, APHP, Paris, France;
      Service Immunologie-Hématologie Pédiatrique, Hôpital Necker-Enfants Malades, APHP,
      Paris, France; Imagine Institut INSERM UMR1163, Université Paris Descartes, Paris,
      France.
FAU - Givel, Claire
AU  - Givel C
AD  - Service de Pneumologie, Hôpital Foch, Suresnes, France; Faculté des Sciences de la
      Santé Simone Veil, Université Versailles-Saint-Quentin-en-Yvelines, Versailles,
      France.
FAU - Castelle, Martin
AU  - Castelle M
AD  - Service d'Hématologie, Hôpital Necker-Enfants Malades, APHP, Paris, France.
FAU - Picard, Capucine
AU  - Picard C
AD  - Centre d'Etude des Déficits Immunitaires (CEDI), Hôpital Necker-Enfants Malades,
      APHP, Paris, France; CEREDIH, Centre de Référence des Déficits Immunitaires
      Héréditaires, Hôpital Universitaire Necker-Enfants Malades, APHP, Paris, France;
      Service Immunologie-Hématologie Pédiatrique, Hôpital Necker-Enfants Malades, APHP,
      Paris, France; Imagine Institut INSERM UMR1163, Université Paris Descartes, Paris,
      France.
FAU - Chansdesris, Marie Olivia
AU  - Chansdesris MO
AD  - Service d'Hématologie, Hôpital Necker-Enfants Malades, APHP, Paris, France.
FAU - Lortholary, Olivier
AU  - Lortholary O
AD  - Service de Maladies Infectieuses et Tropicales, Hôpital Necker-Enfants Malades,
      Assistance Publique-Hôpitaux de Paris (APHP), Université Paris Descartes, Paris,
      France; Institut Pasteur, CNRS, Centre National de Référence Mycoses Invasives et
      Antifongiques, Unité de Mycologie Moléculaire, Paris, France.
FAU - Lanternier, Fanny
AU  - Lanternier F
AD  - Service de Maladies Infectieuses et Tropicales, Hôpital Necker-Enfants Malades,
      Assistance Publique-Hôpitaux de Paris (APHP), Université Paris Descartes, Paris,
      France; Institut Pasteur, CNRS, Centre National de Référence Mycoses Invasives et
      Antifongiques, Unité de Mycologie Moléculaire, Paris, France. Electronic address:
      fanny.lanternier@aphp.fr.
CN  - French Mycoses Study Group
LA  - eng
PT  - Journal Article
DEP - 20190313
PL  - United States
TA  - J Allergy Clin Immunol Pract
JT  - The journal of allergy and clinical immunology. In practice
JID - 101597220
SB  - IM
OTO - NOTNLM
OT  - *Allergic bronchopulmonary aspergillosis
OT  - *Aspergilloma
OT  - *Aspergillosis
OT  - *Cavitary chronic pulmonary aspergillosis
OT  - *STAT3-deficient patient
FIR - Coignard, H
IR  - Coignard H
FIR - Amazzough, K
IR  - Amazzough K
FIR - Suarez, F
IR  - Suarez F
FIR - Blanche, S
IR  - Blanche S
FIR - Sendid, B
IR  - Sendid B
FIR - Cornu, M
IR  - Cornu M
FIR - Bervar, J F
IR  - Bervar JF
FIR - Deschildre, A
IR  - Deschildre A
FIR - Wemeau, L
IR  - Wemeau L
FIR - Fieschi, C
IR  - Fieschi C
FIR - Alanio, A
IR  - Alanio A
FIR - Menetrey, C
IR  - Menetrey C
FIR - Senechal, A
IR  - Senechal A
FIR - Ader, F
IR  - Ader F
FIR - Tattevin, P
IR  - Tattevin P
FIR - Pison, C
IR  - Pison C
FIR - Grandiere-Perez, L
IR  - Grandiere-Perez L
FIR - Garcia-Hermoso, D
IR  - Garcia-Hermoso D
FIR - Botterel-Chartier, F
IR  - Botterel-Chartier F
EDAT- 2019/03/18 06:00
MHDA- 2019/03/18 06:00
CRDT- 2019/03/18 06:00
PHST- 2018/10/09 00:00 [received]
PHST- 2019/02/26 00:00 [revised]
PHST- 2019/02/28 00:00 [accepted]
PHST- 2019/03/18 06:00 [pubmed]
PHST- 2019/03/18 06:00 [medline]
PHST- 2019/03/18 06:00 [entrez]
AID - S2213-2198(19)30263-6 [pii]
AID - 10.1016/j.jaip.2019.02.041 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol Pract. 2019 Jul-Aug;7(6):1986-1995.e3. doi:
      10.1016/j.jaip.2019.02.041. Epub 2019 Mar 13.

PMID- 32176772
OWN - NLM
STAT- In-Process
LR  - 20200731
IS  - 1537-6591 (Electronic)
IS  - 1058-4838 (Print)
IS  - 1058-4838 (Linking)
VI  - 71
IP  - 15
DP  - 2020 Jul 28
TI  - Clinical Features of 69 Cases With Coronavirus Disease 2019 in Wuhan, China.
PG  - 769-777
LID - 10.1093/cid/ciaa272 [doi]
LID - ciaa272
AB  - BACKGROUND: From December 2019 to February 2020, 2019 severe acute respiratory
      syndrome coronavirus 2 (SARS-CoV-2) has caused a serious outbreak of coronavirus
      disease 2019 (COVID-19) in Wuhan, China. Related clinical features are needed.
      METHODS: We reviewed 69 patients who were hospitalized in Union hospital in Wuhan
      between 16 January and 29 January 2020. All patients were confirmed to be infected
      with SARS-CoV-2, and the final date of follow-up was 4 February 2020. RESULTS: The
      median age of 69 enrolled patients was 42.0 years (interquartile range 35.0-62.0),
      and 32 patients (46%) were men. The most common symptoms were fever (60 [87%]),
      cough (38 [55%]), and fatigue (29 [42%]). Most patients received antiviral therapy
      (66 [98.5%] of 67 patients) and antibiotic therapy (66 [98.5%] of 67 patients). As
      of 4 February 2020, 18 (26.9%) of 67 patients had been discharged, and 5 patients
      had died, with a mortality rate of 7.5%. According to the lowest SpO2 during
      admission, cases were divided into the SpO2 ≥ 90% group (n = 55) and the SpO2 < 90%
      group (n = 14). All 5 deaths occurred in the SpO2 < 90% group. Compared with SpO2 ≥
      90% group, patients of the SpO2 < 90% group were older and showed more comorbidities
      and higher plasma levels of interleukin (IL) 6, IL10, lactate dehydrogenase, and C
      reactive protein. Arbidol treatment showed tendency to improve the discharging rate
      and decrease the mortality rate. CONCLUSIONS: COVID-19 appears to show frequent
      fever, dry cough, and increase of inflammatory cytokines, and induced a mortality
      rate of 7.5%. Older patients or those with underlying comorbidities are at higher
      risk of death.
CI  - © The Author(s) 2020. Published by Oxford University Press for the Infectious
      Diseases Society of America. All rights reserved. For permissions, e-mail:
      journals.permissions@oup.com.
FAU - Wang, Zhongliang
AU  - Wang Z
AD  - Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of
      Science and Technology, Wuhan, China.
FAU - Yang, Bohan
AU  - Yang B
AD  - Department of Respiratory and Critical Care Medicine, Union Hospital, Tongji Medical
      College, Huazhong University of Science and Technology, Wuhan, China.
FAU - Li, Qianwen
AU  - Li Q
AD  - Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of
      Science and Technology, Wuhan, China.
FAU - Wen, Lu
AU  - Wen L
AD  - Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of
      Science and Technology, Wuhan, China.
FAU - Zhang, Ruiguang
AU  - Zhang R
AD  - Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of
      Science and Technology, Wuhan, China.
LA  - eng
PT  - Journal Article
TA  - Clin Infect Dis
JT  - Clinical infectious diseases : an official publication of the Infectious Diseases
      Society of America
JID - 9203213
SB  - IM
PMC - PMC7184452
OTO - NOTNLM
OT  - *Wuhan
OT  - *coronavirus
OT  - *pneumonia
EDAT- 2020/03/17 06:00
MHDA- 2020/03/17 06:00
CRDT- 2020/03/17 06:00
PHST- 2020/02/17 00:00 [received]
PHST- 2020/03/12 00:00 [accepted]
PHST- 2020/03/17 06:00 [pubmed]
PHST- 2020/03/17 06:00 [medline]
PHST- 2020/03/17 06:00 [entrez]
AID - 5807944 [pii]
AID - ciaa272 [pii]
AID - 10.1093/cid/ciaa272 [doi]
PST - ppublish
SO  - Clin Infect Dis. 2020 Jul 28;71(15):769-777. doi: 10.1093/cid/ciaa272.

PMID- 31616411
OWN - NLM
STAT- In-Process
LR  - 20200424
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 10
DP  - 2019
TI  - Imbalance of Circulating Innate Lymphoid Cell Subpopulations in Patients With Septic
      Shock.
PG  - 2179
LID - 10.3389/fimmu.2019.02179 [doi]
LID - 2179
AB  - Background: Septic shock, a major cause of death in critical care, is the clinical
      translation of a cytokine storm in response to infection. It can be complicated by
      sepsis-induced immunosuppression, exemplified by blood lymphopenia, an excess of
      circulating Treg lymphocytes, and decreased HLA-DR expression on circulating
      monocytes. Such immunosuppression is associated with secondary infections, and
      higher mortality. The effect of these biological modifications on circulating innate
      lymphoid cells (ILCs) has been little studied. Methods: We prospectively enrolled
      patients with septic shock (Sepsis-3 definition) in the intensive care unit (ICU) of
      Timone CHU Hospital. ICU controls (trauma, cardiac arrest, neurological dysfunction)
      were recruited at the same time (NCT03297203). We performed immunophenotyping of
      adaptive lymphocytes (CD3(+) T cells, CD19(+) B cells, CD4(+)CD25(+)FoxP3(+) Treg
      lymphocytes), ILCs (CD3(-)CD56(+) NK cells and helper ILCs - ILC1, ILC2, and ILC3),
      and monocytes by flow cytometry on fresh blood samples collected between 24 and 72 h
      after admission. Results: We investigated adaptive and innate circulating lymphoid
      cells in the peripheral blood of 18 patients in septic shock, 15 ICU controls, and
      30 healthy subjects. As expected, the peripheral blood lymphocytes of all ICU
      patients showed lymphopenia, which was not specific to sepsis, whereas those of the
      healthy volunteers did not. Circulating CD3(+) T cells and CD3(-)CD56(+) NK cells
      were mainly concerned. There was a tendency toward fewer Treg lymphocytes and lower
      HLA-DR expression on monocytes in ICU patients with sepsis. Although the ILC1 count
      was higher in septic patients than healthy subjects, ILC2, and ILC3 counts were
      lower in both ICU groups. However, ILC3s within the total ILCs were overrepresented
      in patients with septic shock. The depression of immune responses has been
      correlated with the occurrence of secondary infections. We did not find any
      differences in ILC distribution according to this criterion. Conclusion: All ICU
      patients exhibit lymphopenia, regardless of the nature (septic or sterile) of the
      initial medical condition. Specific distribution of circulating ILCs, with an excess
      of ILC1, and a lack of ILC3, may characterize septic shock during the first 3 days
      of the disease.
CI  - Copyright © 2019 Carvelli, Piperoglou, Bourenne, Farnarier, Banzet, Demerlé,
      Gainnier and Vély.
FAU - Carvelli, Julien
AU  - Carvelli J
AD  - APHM, Service de Médecine Intensive et Réanimation, Réanimation Des Urgences,
      Hôpital la Timone, Marseille, France.
AD  - CEReSS - Center for Studies and Research on Health Services and Quality of Life
      EA3279, Aix-Marseille University, Marseille, France.
FAU - Piperoglou, Christelle
AU  - Piperoglou C
AD  - APHM, Hôpital de la Timone, Service d'Immunologie, Marseille Immunopôle, Marseille,
      France.
AD  - Aix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
FAU - Bourenne, Jeremy
AU  - Bourenne J
AD  - APHM, Service de Médecine Intensive et Réanimation, Réanimation Des Urgences,
      Hôpital la Timone, Marseille, France.
AD  - CEReSS - Center for Studies and Research on Health Services and Quality of Life
      EA3279, Aix-Marseille University, Marseille, France.
FAU - Farnarier, Catherine
AU  - Farnarier C
AD  - APHM, Hôpital de la Timone, Service d'Immunologie, Marseille Immunopôle, Marseille,
      France.
FAU - Banzet, Nathalie
AU  - Banzet N
AD  - APHM, Hôpital de la Timone, Service d'Immunologie, Marseille Immunopôle, Marseille,
      France.
FAU - Demerlé, Clemence
AU  - Demerlé C
AD  - APHM, Hôpital de la Timone, Service d'Immunologie, Marseille Immunopôle, Marseille,
      France.
FAU - Gainnier, Marc
AU  - Gainnier M
AD  - APHM, Service de Médecine Intensive et Réanimation, Réanimation Des Urgences,
      Hôpital la Timone, Marseille, France.
AD  - CEReSS - Center for Studies and Research on Health Services and Quality of Life
      EA3279, Aix-Marseille University, Marseille, France.
FAU - Vély, Frédéric
AU  - Vély F
AD  - APHM, Hôpital de la Timone, Service d'Immunologie, Marseille Immunopôle, Marseille,
      France.
AD  - Aix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
LA  - eng
SI  - ClinicalTrials.gov/NCT03297203
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190920
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
SB  - IM
PMC - PMC6763762
OTO - NOTNLM
OT  - *NK cells
OT  - *immunosuppression
OT  - *innate lymphoid cells (ILC)
OT  - *lymphopenia
OT  - *sepsis
OT  - *sepsis-induced immunosuppression
OT  - *septic shock
EDAT- 2019/10/17 06:00
MHDA- 2019/10/17 06:00
CRDT- 2019/10/17 06:00
PHST- 2019/02/18 00:00 [received]
PHST- 2019/08/29 00:00 [accepted]
PHST- 2019/10/17 06:00 [entrez]
PHST- 2019/10/17 06:00 [pubmed]
PHST- 2019/10/17 06:00 [medline]
AID - 10.3389/fimmu.2019.02179 [doi]
PST - epublish
SO  - Front Immunol. 2019 Sep 20;10:2179. doi: 10.3389/fimmu.2019.02179. eCollection 2019.

PMID- 31638924
OWN - NLM
STAT- In-Process
LR  - 20200513
IS  - 1471-2431 (Electronic)
IS  - 1471-2431 (Linking)
VI  - 19
IP  - 1
DP  - 2019 Oct 21
TI  - Mutations in both SAMD9 and SLC19A2 genes caused complex phenotypes characterized by
      recurrent infection, dysphagia and profound deafness - a case report for dual
      diagnosis.
PG  - 364
LID - 10.1186/s12887-019-1733-y [doi]
LID - 364
AB  - BACKGROUND: Phenotypic difference is general in Mendelian disease. Due to the
      extremely low incidence for a single disease, phenotype spectrum needs to be
      expanded. Meanwhile, earlier knowledge says patients who suffered from two kinds of
      different Mendelian disease are very rare. CASE PRESENTATION: We describe a case of
      neonatal male with genital anomalies, growth delay, skin hyperpigmentation, chronic
      lung disease with recurrent infection, anemia, and severe deafness. Without any
      clear etiology after routine workflow, whole exome sequencing was carried on. A
      pathogenic de novo SAMD9 mutation and compound heterozygous likely-pathogenic
      variants in SLC19A2 were identified. Some symptoms were improved after the patient
      was treated with vitamin B1. Unfortunately, the boy died from sepsis and multiple
      organ failure before 1 year old. CONCLUSION: Combining the phenotype and clinical
      progress of treatment, we report that it is the first case of a patient with both
      MIRAGE syndrome and TRMA syndrome.
FAU - Zhang, Yan
AU  - Zhang Y
AD  - Center for Medical Genetics, Guangdong Women and Children Hospital, 521
      Xingnandadao, Guangzhou, 511442, China.
FAU - Zhang, Yi
AU  - Zhang Y
AD  - Euler Genomics Co. Ltd., Beijing, China.
FAU - Zhang, Victor Wei
AU  - Zhang VW
AD  - AmCare Genomics Laboratory, Guangzhou, China.
AD  - Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX,
      USA.
FAU - Zhang, Chunyi
AU  - Zhang C
AD  - Neonatology Department, Guangdong Women and Children Hospital, Guangzhou, China.
FAU - Ding, Hongke
AU  - Ding H
AD  - Center for Medical Genetics, Guangdong Women and Children Hospital, 521
      Xingnandadao, Guangzhou, 511442, China.
FAU - Yin, Aihua
AU  - Yin A
AUID- ORCID: 0000-0002-0324-5260
AD  - Center for Medical Genetics, Guangdong Women and Children Hospital, 521
      Xingnandadao, Guangzhou, 511442, China. yinaiwa@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191021
TA  - BMC Pediatr
JT  - BMC pediatrics
JID - 100967804
SB  - IM
PMC - PMC6802302
OTO - NOTNLM
OT  - *Familial
OT  - *High-throughput nucleotide sequencing
OT  - *MIRAGE syndrom
OT  - *Normophosphatemic
OT  - *Thiamine responsive megaloblastic anemia syndrome
OT  - *Tumoral calcinosis
COIS- The authors declare that they have no competing interests.
EDAT- 2019/10/23 06:00
MHDA- 2019/10/23 06:00
CRDT- 2019/10/23 06:00
PHST- 2018/12/11 00:00 [received]
PHST- 2019/09/20 00:00 [accepted]
PHST- 2019/10/23 06:00 [entrez]
PHST- 2019/10/23 06:00 [pubmed]
PHST- 2019/10/23 06:00 [medline]
AID - 10.1186/s12887-019-1733-y [pii]
AID - 1733 [pii]
AID - 10.1186/s12887-019-1733-y [doi]
PST - epublish
SO  - BMC Pediatr. 2019 Oct 21;19(1):364. doi: 10.1186/s12887-019-1733-y.

PMID- 30988361
OWN - NLM
STAT- In-Process
LR  - 20200414
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 9
IP  - 1
DP  - 2019 Apr 15
TI  - Selenium nanoparticles for targeted stroke therapy through modulation of
      inflammatory and metabolic signaling.
PG  - 6044
LID - 10.1038/s41598-019-42633-9 [doi]
LID - 6044
AB  - Ischemic cerebral stroke is a major cause of death and morbidity. Currently, no
      neuroprotective agents have been shown to impact the clinical outcomes in cerebral
      stroke cases. Here, we report therapeutic effects of Se nanoparticles on ischemic
      stroke in a murine model. Anti-transferrin receptor monoclonal antibody
      (OX26)-PEGylated Se nanoparticles (OX26-PEG-Se NPs) were designed and synthesized
      and their neuroprotective effects were measured using in vitro and in vivo
      approaches. We demonstrate that administration of the biodegradable nanoparticles
      leads to resolution of brain edema, protection of axons in hippocampus region, and
      myelination of hippocampal area after cerebral ischemic stroke. Our nanoparticle
      design ensures efficient targeting and minimal side effects. Hematological and
      biochemical analyses revealed no undesired NP-induced changes. To gain mechanistic
      insights into the therapeutic effects of these particles, we characterized the
      changes to the relevant inflammatory and metabolic signaling pathways. We assessed
      metabolic regulator mTOR and related signaling pathways such as hippo,
      Ubiquitin-proteasome system (ERK5), Tsc1/Tsc2 complex, FoxO1, wnt/β-catenine
      signaling pathway. Moreover, we examined the activity of jak2/stat3 signaling
      pathways and Adamts1, which are critically involved in inflammation. Together, our
      study provides a promising treatment strategy for cerebral stroke based on Se NP
      induced suppression of excessive inflammation and oxidative metabolism.
FAU - Amani, Hamed
AU  - Amani H
AUID- ORCID: 0000-0002-9092-5642
AD  - Department of medical nanotechnology, Faculty of Advanced Technologies in Medicine,
      Iran University of Medical Science, Tehran, Iran.
FAU - Habibey, Rouhollah
AU  - Habibey R
AD  - Department of Neuroscience and Brain Technologies-Istituto Italiano di Technologia,
      Via Morego, Genova, Italy.
FAU - Shokri, Fereshteh
AU  - Shokri F
AD  - International Pharmaceutical Federation, The Hague, Netherlands.
FAU - Hajmiresmail, Seyed Javad
AU  - Hajmiresmail SJ
AD  - Department of Cardiology, Iran University of Medical Sciences, Tehran, Iran.
FAU - Akhavan, Omid
AU  - Akhavan O
AD  - Department of Physics, Sharif University of Technology, Tehran, Iran.
      oakhavan@sharif.edu.
FAU - Mashaghi, Alireza
AU  - Mashaghi A
AD  - Leiden Academic Centre for Drug Research, Faculty of Science, Leiden University,
      Leiden, Netherlands. a.mashaghi.tabari@lacdr.leidenuniv.nl.
AD  - Harvard Medical School, Harvard University, Boston, USA.
      a.mashaghi.tabari@lacdr.leidenuniv.nl.
FAU - Pazoki-Toroudi, Hamidreza
AU  - Pazoki-Toroudi H
AD  - Physiology Research Center and Department of Physiology, Faculty of Medicine, Iran
      University of Medical Sciences, Tehran, Iran. pazoki.h@iums.ac.ir.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190415
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
PMC - PMC6465364
COIS- The authors declare no competing interests.
EDAT- 2019/04/17 06:00
MHDA- 2019/04/17 06:00
CRDT- 2019/04/17 06:00
PHST- 2018/10/04 00:00 [received]
PHST- 2019/04/03 00:00 [accepted]
PHST- 2019/04/17 06:00 [entrez]
PHST- 2019/04/17 06:00 [pubmed]
PHST- 2019/04/17 06:00 [medline]
AID - 10.1038/s41598-019-42633-9 [pii]
AID - 42633 [pii]
AID - 10.1038/s41598-019-42633-9 [doi]
PST - epublish
SO  - Sci Rep. 2019 Apr 15;9(1):6044. doi: 10.1038/s41598-019-42633-9.