Update data

data/STRchive-disease-loci.T2T-chm13.bed

@@ -9,7 +9,7 @@ chr2	100563686	100563738	FRA2A_AFF3	AFF3	GCC	300	AD	Intellectual disability asso
 chr2	176581179	176581220	SD5_HOXD13	HOXD13	GCN	22	AD	Syndactyly
 chr2	191369983	191370024	GDPAG_GLS	GLS	GCA	680	AR	Glutaminase deficiency
 chr3	63956303	63956334	SCA7_ATXN7	ATXN7	CAG	37	AD	Spinocerebellar Ataxia Type 7
-chr3	131917483	131917557	DM2_CNBP	CNBP	CAGG	75	AD	Myotonic Dystrophy Type 2
+chr3	131917483	131917557	DM2_CNBP	CNBP	CAGG,CAGA	75	AD	Myotonic Dystrophy Type 2
 chr3	141687014	141687051	BPES_FOXL2	FOXL2	NGC	15	AD,AR	Blepharophimosis, epicanthus inversus, and ptosis
 chr3	186521657	186521706	FAME4_YEATS2	YEATS2	TTTCA	1000	AD	Familial adult myoclonic epilepsy 4
 chr4	3073604	3073694	HD_HTT	HTT	CAG	40	AD	Huntington disease

data/STRchive-disease-loci.hg19.bed

@@ -9,7 +9,7 @@ chr2	100721261	100721286	FRA2A_AFF3	AFF3	GCC	300	AD	Intellectual disability asso
 chr2	176957786	176957831	SD5_HOXD13	HOXD13	GCN	22	AD	Syndactyly
 chr2	191745599	191745646	GDPAG_GLS	GLS	GCA	680	AR	Glutaminase deficiency
 chr3	63898361	63898392	SCA7_ATXN7	ATXN7	CAG	37	AD	Spinocerebellar Ataxia Type 7
-chr3	128891420	128891502	DM2_CNBP	CNBP	CAGG	75	AD	Myotonic Dystrophy Type 2
+chr3	128891420	128891502	DM2_CNBP	CNBP	CAGG,CAGA	75	AD	Myotonic Dystrophy Type 2
 chr3	138664862	138664904	BPES_FOXL2	FOXL2	NGC	15	AD,AR	Blepharophimosis, epicanthus inversus, and ptosis
 chr3	183429976	183430010	FAME4_YEATS2	YEATS2	TTTCA	1000	AD	Familial adult myoclonic epilepsy 4
 chr4	3076604	3076667	HD_HTT	HTT	CAG	40	AD	Huntington disease

data/STRchive-disease-loci.hg38.bed

@@ -9,7 +9,7 @@ chr2	100104799	100104824	FRA2A_AFF3	AFF3	GCC	300	AD	Intellectual disability asso
 chr2	176093058	176093103	SD5_HOXD13	HOXD13	GCN	22	AD	Syndactyly
 chr2	190880873	190880920	GDPAG_GLS	GLS	GCA	680	AR	Glutaminase deficiency
 chr3	63912685	63912716	SCA7_ATXN7	ATXN7	CAG	37	AD	Spinocerebellar Ataxia Type 7
-chr3	129172577	129172659	DM2_CNBP	CNBP	CAGG	75	AD	Myotonic Dystrophy Type 2
+chr3	129172577	129172659	DM2_CNBP	CNBP	CAGG,CAGA	75	AD	Myotonic Dystrophy Type 2
 chr3	138946020	138946062	BPES_FOXL2	FOXL2	NGC	15	AD,AR	Blepharophimosis, epicanthus inversus, and ptosis
 chr3	183712188	183712222	FAME4_YEATS2	YEATS2	TTTCA	1000	AD	Familial adult myoclonic epilepsy 4
 chr4	3074877	3074940	HD_HTT	HTT	CAG	40	AD	Huntington disease

data/STRchive-loci.json

@@ -681,7 +681,7 @@
   "mechanism": "GoF",
   "mechanism_detail": "Polyglutamine expansion leading to gain of function; aggregated and mislocalized proteins in neurons [@pmid:36169768; @genereviews:NBK1196].",
   "source": [],
-  "details": "Benign alleles range from 11-44 repeats [@pmid:37906407], with intermediate alleles (45-59) associated with incomplete penetrance and non-classic phenotypes [@genereviews:NBK1196]. The threshold between incomplete and full penetrance is unclear, but presumed to occur at ~60 repeats [@genereviews:NBK1196; @pmid:37906407]. The interruption CAA has been observed [@pmid:35245110]; AAG is present in hg38 reference sequence.",
+  "details": "Benign alleles range from 11-44 repeats [@pmid:37906407], with intermediate alleles (45-59) associated with incomplete penetrance and non-classic phenotypes [@genereviews:NBK1196]. The threshold between incomplete and full penetrance is unclear, but presumed to occur at ~60 repeats [@genereviews:NBK1196; @pmid:37906407]. The interruption CAA has been observed [@pmid:35245110]; AAG is present in hg38 reference sequence. The APOE ε4 allele appears to act as a disease modifier [@pmid:39731318]; GLS expansions may also function as disease modifiers [@pmid: 39699045].",
   "omim": ["109150"],
   "prevalence": "2.1/100000",
   "prevalence_details": "1-5/100,000 [@pmid:29100084]. Most prevalent SCA subtype [@genereviews:NBK557816]. Found worldwide across ancestries/ethnicities [@genereviews:NBK1196].",
@@ -925,7 +925,7 @@
   "intermediate_min": 24.0,
   "intermediate_max": 60.0,
   "pathogenic_min": 251.0,
-  "pathogenic_max": 4000.0,
+  "pathogenic_max": 4088.0,
   "ref_copies": 10.8,
   "motif_len": 6,
   "age_onset": "Typical: 50-64; Range: 20-91 [@genereviews:NBK268647].",
@@ -937,7 +937,7 @@
   "mechanism": "Ambiguous",
   "mechanism_detail": "The HRE forms DNA and RNA G-quadruplexes with distinct structures and promotes RNA/DNA hybrids (R-loops). The structural polymorphism causes a repeat length-dependent accumulation of transcripts aborted in the HRE region [@omim:105500]. Addiitonal mechanisms theorized include protein loss of function and RNA gain of function [@pmid:37847372].",
   "source": [],
-  "details": "FTD and ALS form a clinical spectrum [@pmid:37388914; @pmid:22406228]. The clinical ranges of the C9orf72 locus remain ambiguous [@stripy:C9ORF72]: most healthy controls have alleles up to 24 repeats [@pmid:28319737] yet 24-30 repeats are associated with ALS [@pmid:31315673] and while 60 repeats is frequently used as a threshold for uncertain alleles, the exact threshold of pathogenicity remains unclear [@genereviews:NBK268647; @pmid:38099605]. Repeat of 80 motifs and lower appear to have delayed onset for any phenotype [@pmid:28319737]. >250 repeats are associated with a full FTD/ALS disease state [@pmid:31048495], but pathogenic alleles can range from 30 to more than 4000 repeats [@pmid:38099605]. Penetrance appears to also be age-dependent, with environmental factors and specific phenotypes associated with sex and age at onset [@pmid:28522837].",
+  "details": "FTD and ALS form a clinical spectrum [@pmid:37388914; @pmid:22406228]. The clinical ranges of the C9orf72 locus remain ambiguous [@stripy:C9ORF72]: most healthy controls have alleles up to 24 repeats [@pmid:28319737] yet 24-30 repeats are associated with ALS [@pmid:31315673] and while 60 repeats is frequently used as a threshold for uncertain alleles, the exact threshold of pathogenicity remains unclear [@genereviews:NBK268647; @pmid:38099605]. Repeat of 80 motifs and lower appear to have delayed onset for any phenotype [@pmid:28319737]. >250 repeats are associated with a full FTD/ALS disease state [@pmid:31048495], but pathogenic alleles can range from 30 to more than 4000 repeats [@pmid:38099605; @pmid:39709476]. Penetrance appears to also be age-dependent, with environmental factors and specific phenotypes associated with sex and age at onset [@pmid:28522837]. Methylation appears to increase with expansion length and age [@pmid:39709476].",
   "omim": ["105500"],
   "prevalence": null,
   "prevalence_details": "The expansion of a hexanucleotide repeat GGGGCC in C9orf72 is the most common known cause of ALS accounting for ~ 40% familial cases and ~ 7% sporadic cases in the European population; overall ALS incidence is 1-2/100,000 person-years, point prevalence is 3-5/100,000 (Europe/US); lifetime risk is 1 in 300 [@pmid:31315673]. Related individuals to patients with C9orf72-ALS appear at an increased risk of disease regardless of carrier status [@pmid:38149039; @pmid:39315390]. C9orf72-FTD is estimated to be 0.04-134:100,000 [@genereviews:NBK268647], and by our estimates 0.65-1.56/100,000 for C9orf72-ALS. The expansion has been found across ethnicities/ancestries, with population-dependent prevalence, highest in those with northern European ancestry [@genereviews:NBK268647].",
@@ -1099,8 +1099,8 @@
   "disease_id": "DM2",
   "gene_strand": "-",
   "reference_motif_reference_orientation": ["CAGG"],
-  "pathogenic_motif_reference_orientation": ["CAGG"],
-  "pathogenic_motif_gene_orientation": ["CCTG"],
+  "pathogenic_motif_reference_orientation": ["CAGG", "CAGA"],
+  "pathogenic_motif_gene_orientation": ["CCTG", "CTGT"],
   "benign_motif_reference_orientation": [],
   "benign_motif_gene_orientation": [],
   "unknown_motif_reference_orientation": [],
@@ -1129,7 +1129,7 @@
   "mechanism": "GoF",
   "mechanism_detail": "Aberrant splicing, RAN translation [@pmid:22140091; @pmid:38467784].",
   "source": [],
-  "details": "Detailed overview of disease locus through 2024 by Rimoldi et al [@pmid:39643839]. ≤30 uninterrupted CCTG repeats or 11-26 CCTG repeats with GCTC/TCTG interruptions are considered benign; 27-29 repeats with interruptions have currently unknown significance, ~30-~54 repeats are considered premutations, ~55-74 repeats are premutations with possible reduced penetrance, and >74 repeat alleles are considered pathogenic [@genereviews:NBK1466]. Penetrance is age-dependent and approaches 100%. Locus structure is (TG)n(TCTG)n(CCTG)n. CCTG expansion causes DM2 but the other repeat units are also variable. Interruptions include GCTG/TCTG/GGCT [@pmid:35245110].",
+  "details": "Detailed overview of disease locus through 2024 by Rimoldi et al [@pmid:39643839]. ≤30 uninterrupted CCTG repeats or 11-26 CCTG repeats with GCTC/TCTG interruptions are considered benign; 27-29 repeats with interruptions have currently unknown significance, ~30-~54 repeats are considered premutations, ~55-74 repeats are premutations with possible reduced penetrance, and >74 repeat alleles are considered pathogenic [@genereviews:NBK1466]. Penetrance is age-dependent and approaches 100%. Locus structure is (TG)n(TCTG)n(CCTG)n. CCTG expansion causes DM2 but the other repeat units are also variable. Interruptions include GCTG/TCTG/GGCT [@pmid:35245110; @pmid:39703464].",
   "omim": ["602668"],
   "prevalence": "2.29/100000",
   "prevalence_details": "2.29/100,000 [@pmid:35483324]; population specific prevalence [@genereviews:NBK1466]. Most cases have European ancestry, but disease has been reported worldwide [@genereviews:NBK1466].",
@@ -1513,7 +1513,7 @@
   "mechanism": "GoF",
   "mechanism_detail": "RNA gain-of-function: RNA gelation leading to misregulation of alternative splicing [@pmid:36169768].",
   "source": [],
-  "details": "Overview of disease locus through 2024, including largest pathogenic allele of 4,000, described in Rimoldi et al review [@pmid:39643839]. Intermediate alleles (35-49) associated with premutation [@genereviews:NBK1165]. 3%-8% of DM1 expansions contain variant repeats such as CCG and CGG, associated with later onset and milder phenotype [@pmid:32851192]. In another study, interruptions of the CTG repeat with CCG, GGC, CTC or CAG motifs are estimated to occur in 3-11% of DM1 patients [@pmid:35741732].",
+  "details": "Overview of disease locus through 2024, including largest pathogenic allele of 4,000, described in Rimoldi et al review [@pmid:39643839]. Intermediate alleles (35-49) associated with premutation [@genereviews:NBK1165]. 3%-8% of DM1 expansions contain interrupting variant repeats such as CCG and CGG, associated with later onset and milder phenotype; the variant repeat GCGGCA has also been reported [@pmid:32851192; @doi:10.1016/j.mcp.2024.102005]. In another study, interruptions of the CTG repeat with CCG, GGC, CTC or CAG motifs are estimated to occur in 3-11% of DM1 patients [@pmid:35741732]. Expansions within gene ZNF850 may function as DM1 modifiers [@doi:10.1093/hmg/ddae186].",
   "omim": ["160900"],
   "prevalence": "9.27/100000",
   "prevalence_details": "5-20/100,000 [@genereviews:NBK1165]. 0.5-18.1/100,000 [@pmid:29100084]; 6.5/100,000 [@pmid:31159885]. 9.27 cases (95% CI: 4.73-15.21) per 100,000, ranging from 0.37 to 36.29 cases per 100,000 [@pmid:35483324]. Found across ethnicities/ancestries, with population-dependent prevalence [@genereviews:NBK1165].",
@@ -4012,7 +4012,7 @@
   "details": "Most controls have <40 repeats while majority of patients have >50 repeats; penetrance is <100%, as unaffected individuals have been documented with >80 repeats and alleles of affected individuals range from 12-2600 [@genereviews:NBK535148; @pmid:25168903]. Expansions are causative in approximately 70% of disease cases [@genereviews:NBK535148].",
   "omim": ["613267"],
   "prevalence": "4.5/100",
-  "prevalence_details": "~4/100 (over 40) [@omim:613267]; 5/100 [@pmid:20825314]. Predominantly in women (~75%) [@pmid:16769829]. Although studies on the prevalence of FECD worldwide are limited, the disorder is thought to be more common in Eurasian populations [@pmid:26401622], with its corneal manifestations documented in 11% of females and 7% of males in Reykjavik, Iceland, 8.5 % of Singapore Chinese, and 5.5% of Japanese [@pmid:25722209]. Uncommon/rare in Saudi Arabia, Singaporean Chinese, and Japan [@orphanet:98974].",
+  "prevalence_details": "~4/100 (over 40) [@omim:613267]; 5/100 [@pmid:20825314]. Predominantly in women (~75%) [@pmid:16769829]. In one study of two cohorts (Dallas Heart Study and 1000 Genomes Project), expanded allele carrier rates were 3.1% (African American), 8.1% (European American), and 3.3% (Latinos)in DHS, and 2.7% (AFR), 9.5% (EUR), 5.2% (East Asians), 7.2% (South Asians), and 5.2% (admixed Americans) in 1KGP [@pmid:39669694]. The highest carrier prevalence (12.1%–12.5%) occurred in EUR and admixed American subpopulations, while rates were 0%–1.9% in West Africans vs 6.2% in a Kenyan subpopulation.",
   "stripy": ["TCF4"],
   "gnomad": ["TCF4"],
   "genereviews": ["NBK535148"],

data/literature/AR01.txt

@@ -10083,7 +10083,7 @@ PMID- 30247609
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20191212
-LR  - 20241218
+LR  - 20241227
 IS  - 1945-7197 (Electronic)
 IS  - 0021-972X (Linking)
 VI  - 104
@@ -39173,7 +39173,7 @@ PMID- 10732754
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20000405
-LR  - 20241218
+LR  - 20241227
 IS  - 0007-0920 (Print)
 IS  - 1532-1827 (Electronic)
 IS  - 0007-0920 (Linking)

data/literature/ARX01.txt

@@ -1396,7 +1396,7 @@ PMID- 23246292
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20130312
-LR  - 20241218
+LR  - 20241227
 IS  - 1537-6605 (Electronic)
 IS  - 0002-9297 (Print)
 IS  - 0002-9297 (Linking)
@@ -2252,7 +2252,7 @@ PMID- 18462864
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20080829
-LR  - 20241218
+LR  - 20241227
 IS  - 0303-8467 (Print)
 IS  - 0303-8467 (Linking)
 VI  - 110
@@ -2547,7 +2547,7 @@ PMID- 17480217
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20070517
-LR  - 20241218
+LR  - 20241227
 IS  - 1471-2350 (Electronic)
 IS  - 1471-2350 (Linking)
 VI  - 8

data/literature/C9orf7201.txt

@@ -3,7 +3,7 @@ PMID- 39730482
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20241227
-LR  - 20241227
+LR  - 20241231
 IS  - 2045-2322 (Electronic)
 IS  - 2045-2322 (Linking)
 VI  - 14

data/literature/DMPK01.txt

@@ -2,12 +2,13 @@
 PMID- 39710066
 OWN - NLM
 STAT- Publisher
-LR  - 20241222
+LR  - 20241230
 IS  - 1096-1194 (Electronic)
 IS  - 0890-8508 (Linking)
-DP  - 2024 Dec 20
-TI  - High-resolution repeat structure analysis in molecular diagnostics of myotonic 
-      dystrophy type 1 using short-read whole genome sequencing.
+VI  - 79
+DP  - 2024 Dec 29
+TI  - Advancing molecular diagnostics of myotonic dystrophy type 1 using short-read 
+      whole genome sequencing.
 PG  - 102005
 LID - S0890-8508(24)00057-4 [pii]
 LID - 10.1016/j.mcp.2024.102005 [doi]
@@ -29,7 +30,7 @@ AB  - Myotonic dystrophy type 1 (DM1) is a serious multisystem disorder caused b
       expansion-range/premutation-range alleles. Although neither the tested 
       conventional methods, nor WGS allowed expanded-allele sizing, conventional 
       methods provided higher sizing limits for normal-range alleles. Genotyping 
-      concordance rate was found to be 95-99%. WGS was found to be superior in 
+      concordance rate was found to be 95-99 %. WGS was found to be superior in 
       elucidating the sequence structure of the motifs, even if they fall outside the 
       sizing limit (from partial reads). In addition, WGS enables the identification of 
       genetic modifiers in other genes and the detection of alternative diagnoses in 
@@ -62,8 +63,8 @@ FAU - Zatkova, Andrea
 AU  - Zatkova A
 AD  - Institute of Clinical and Translational Research, Biomedical Research Center of 
       the Slovak Academy of Sciences, Bratislava, Slovakia.
-FAU - Tarova, Eva Tothova
-AU  - Tarova ET
+FAU - Tothova Tarova, Eva
+AU  - Tothova Tarova E
 AD  - Institute of Clinical and Translational Research, Biomedical Research Center of 
       the Slovak Academy of Sciences, Bratislava, Slovakia; Department of Biology, 
       Faculty of Education, J. Selye University, Komarno, Slovakia.
@@ -90,19 +91,19 @@ AD  - Institute of Clinical and Translational Research, Biomedical Research Cent
       Slovakia. Electronic address: [email protected].
 LA  - eng
 PT  - Journal Article
-DEP - 20241220
+DEP - 20241229
 PL  - England
 TA  - Mol Cell Probes
 JT  - Molecular and cellular probes
 JID - 8709751
 SB  - IM
 OTO - NOTNLM
-OT  - massively parallel sequencing
-OT  - myotonic dystrophy type 1
-OT  - repeat expansion disorders
-OT  - tandem repeats
-OT  - whole genome sequencing
-COIS- Declaration of Competing Interest ... The authors declare the following financial 
+OT  - Massively parallel sequencing
+OT  - Myotonic dystrophy type 1
+OT  - Repeat expansion disorders
+OT  - Tandem repeats
+OT  - Whole genome sequencing
+COIS- Declaration of competing interest The authors declare the following financial 
       interests/personal relationships which may be considered as potential competing 
       interests:Tomas Szemes reports a relationship with Genovisio Ltd. that includes: 
       equity or stocks. If there are other authors, they declare that they have no 
@@ -114,13 +115,13 @@ CRDT- 2024/12/22 19:14
 PHST- 2024/12/05 00:00 [received]
 PHST- 2024/12/20 00:00 [revised]
 PHST- 2024/12/20 00:00 [accepted]
-PHST- 2024/12/23 00:19 [medline]
 PHST- 2024/12/23 00:19 [pubmed]
+PHST- 2024/12/23 00:19 [medline]
 PHST- 2024/12/22 19:14 [entrez]
 AID - S0890-8508(24)00057-4 [pii]
 AID - 10.1016/j.mcp.2024.102005 [doi]
 PST - aheadofprint
-SO  - Mol Cell Probes. 2024 Dec 20:102005. doi: 10.1016/j.mcp.2024.102005.
+SO  - Mol Cell Probes. 2024 Dec 29;79:102005. doi: 10.1016/j.mcp.2024.102005.
 
 PMID- 39679849
 OWN - NLM
@@ -7928,7 +7929,7 @@ PMID- 33235377
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20220114
-LR  - 20241218
+LR  - 20241227
 IS  - 1476-5438 (Electronic)
 IS  - 1018-4813 (Print)
 IS  - 1018-4813 (Linking)

data/literature/FMR101.txt

@@ -51683,7 +51683,7 @@ PMID- 14560307
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20040506
-LR  - 20241218
+LR  - 20241227
 IS  - 1018-4813 (Print)
 IS  - 1018-4813 (Linking)
 VI  - 12
@@ -53415,7 +53415,7 @@ PMID- 11410685
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20011018
-LR  - 20241218
+LR  - 20241227
 IS  - 1011-8934 (Print)
 IS  - 1598-6357 (Electronic)
 IS  - 1011-8934 (Linking)

data/literature/HTT01.txt

@@ -38408,7 +38408,7 @@ PMID- 32102602
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20210517
-LR  - 20241218
+LR  - 20241227
 IS  - 1545-7222 (Electronic)
 IS  - 0895-0172 (Linking)
 VI  - 32

data/literature/LRP1201.txt

@@ -151,7 +151,7 @@ PMID- 38726482
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20240724
-LR  - 20240724
+LR  - 20241231
 IS  - 2167-9223 (Electronic)
 IS  - 2167-8421 (Linking)
 VI  - 25
@@ -235,19 +235,20 @@ PL  - England
 TA  - Amyotroph Lateral Scler Frontotemporal Degener
 JT  - Amyotrophic lateral sclerosis & frontotemporal degeneration
 JID - 101587185
-RN  - 0 (LDL-Receptor Related Proteins)
+RN  - 0 (LRP12 protein, human)
+RN  - 0 (Low Density Lipoprotein Receptor-Related Protein-1)
 SB  - IM
+MH  - Adult
+MH  - Aged
+MH  - Female
 MH  - Humans
-MH  - *Amyotrophic Lateral Sclerosis/genetics
 MH  - Male
-MH  - Female
-MH  - *White People/genetics
 MH  - Middle Aged
-MH  - Aged
-MH  - Adult
-MH  - LDL-Receptor Related Proteins/genetics
+MH  - *Amyotrophic Lateral Sclerosis/genetics
 MH  - Cohort Studies
-MH  - Trinucleotide Repeat Expansion/genetics
+MH  - Trinucleotide Repeat Expansion
+MH  - *White People/genetics
+MH  - *Low Density Lipoprotein Receptor-Related Protein-1/genetics
 OTO - NOTNLM
 OT  - Amyotrophic lateral sclerosis
 OT  - LRP12

data/literature/RAI101.txt

@@ -537,7 +537,7 @@ PMID- 33186760
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20210608
-LR  - 20241218
+LR  - 20241227
 IS  - 1878-0849 (Electronic)
 IS  - 1769-7212 (Linking)
 VI  - 64
@@ -1232,7 +1232,7 @@ PMID- 23897707
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20140326
-LR  - 20241218
+LR  - 20241227
 IS  - 1552-4833 (Electronic)
 IS  - 1552-4825 (Linking)
 VI  - 161A

data/literature/RFC101.txt

@@ -2850,7 +2850,7 @@ PMID- 38324175
 OWN - NLM
 STAT- MEDLINE
 DCOM- 20240724
-LR  - 20240727
+LR  - 20241231
 IS  - 1473-4230 (Electronic)
 IS  - 1473-4222 (Print)
 IS  - 1473-4222 (Linking)