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Aims: Recently, exosomal miRNAs have been shown to play important roles in multiple diseases, including type 1 diabetes (T1D). To assess the biomarker potential of exosomal miRNAs for T1D, we measured the expression profiles of plasma‐derived exosomal miRNAs in T1D and explored their potential functions by bioinformatic analysis. Materials and methods: In the discovery phase, exosome samples were isolated from plasma by size exclusion chromatography from 10 T1D patients and 10 sex‐ (p = 0.36), age‐ (p = 0.97), and body mass index‐matched (p = 0.47) healthy control subjects. Exosomal miRNA expression profiles were measured using the Illumina NovaSeq 6000 platform. With verification by quantitative real‐time PCR (qRT‒PCR), we used multiple bioinformatics approaches to explore the potential biological functions of the identified differentially expressed miRNAs. The diagnostic signature of exosomal miRNAs was evaluated by least absolute shrinkage and selection operator (LASSO) regression and evaluated based on the area under the receiver operating characteristic curve (AUC). Results: In total, 43 differentially expressed miRNAs, among which 34 were upregulated and 9 were downregulated, were identified in T1D. After correcting for multiple testing using false discovery rate, 11 identified exosomal miRNAs still showed statistical significance. Among the 5 selected miRNAs, 3 miRNAs (miR‐103a‐3p, miR‐144‐5p and miR‐454‐3p) were successfully validated by qRT‒PCR. The biological analysis‐enriched terms included protein autophosphorylation and the Hedgehog signalling pathway. The highest AUC of exosomal miRNA was 0.889 under the LASSO model. The expression levels of 5 selected exosomal miRNAs were correlated with multiple clinical characteristics such as fasting C‐peptide and postprandial C‐peptide. Conclusions: Our results indicated that plasma‐derived exosomal miRNAs could serve as promising diagnostic biomarkers of T1D. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Different types of diabetes show distinct genetic characteristics, but the specific genetic susceptibility factors remain unclear. Our study aimed to explore the associations between the ribosomal protein S26 (RPS26) gene rs1131017 polymorphisms and susceptibility to type 1 diabetes mellitus, latent autoimmune diabetes in adults (LADA) and type 2 diabetes mellitus in the Chinese Han population, and their correlations with clinical features. Materials and Methods: Genotyping of the rs1131017 variant was carried out for 1,006 type 1 diabetes mellitus patients, 210 LADA patients, 642 type 2 diabetes mellitus patients and 2,099 control individuals. Results: We found that the rs1131017 C allele was a risk locus for both type 1 diabetes mellitus and LADA (odds ratio [OR] 1.50, 95% confidence interval [CI] 1.33–1.69, P < 0.001; OR 1.31, 95% CI 1.04–1.64, P = 0.021, respectively). Nevertheless, this association was not found for type 2 diabetes mellitus. Carrying the C allele genotype was associated with a lower postprandial C‐peptide for type 1 diabetes mellitus (OR 1.41, 95% CI 1.11–1.80, P = 0.006) and lower fasting C‐peptide for LADA (OR 1.55, 95% CI 1.01–2.38, P = 0.047). Interestingly, a lower GC frequency was noted for LADA than for type 1 diabetes mellitus, regardless of classification based on age at diagnosis, C‐peptide or glutamic acid decarboxylase antibody positivity. Conclusions: The RPS26 polymorphism was associated with susceptibility and clinical characteristics of type 1 diabetes mellitus and LADA in the Chinese population, but was not related to type 2 diabetes mellitus. Thus, it might serve as a novel biomarker for particular types of diabetes. In this manuscript, we explored whether RPS26 gene polymorphisms conferred susceptibility to type 1 diabetes mellitus, latent autoimmune diabetes in adults and type 2 diabetes mellitus in a considerably large collection of Chinese participants. The effects of this gene on clinical features of patients, including age at diagnosis, β‐cell function, and islet autoantibodies were also comprehensively investigated. We have found that the SNP, rs1131017, of the RPS26 gene is a genetic susceptibility locus for type 1 diabetes mellitus and latent autoimmune diabetes in adults in the Chinese Han population, but it has no impact on susceptibility to type 2 diabetes mellitus. Our research provides evidence for the important role of RPS26 in the genetic susceptibility of type 1 diabetes mellitus, offering a new biomarker for risk assessment and precise diagnosis of diabetes. [ABSTRACT FROM AUTHOR]

Aims: Idiopathic type 1 diabetes (T1D) is a neglected subtype of T1D. Our aim was to investigate the frequency, clinical characteristics, and human leucocyte antigen (HLA) genotypes of idiopathic T1D. Methods: We enrolled 1205 newly diagnosed T1D patients in our analysis. To exclude monogenic diabetes in autoantibody‐negative patients, we utilised a custom monogenic diabetes gene panel. Individuals negative for autoantibodies and subsequently excluded for monogenic diabetes were diagnosed with idiopathic T1D. We collected clinical characteristics, measured islet autoantibodies by radioligand assay and obtained HLA data. Results: After excluding 11 patients with monogenic diabetes, 284 cases were diagnosed with idiopathic T1D, accounting for 23.8% (284/1194) of all newly diagnosed T1D cases. When compared with autoimmune T1D, idiopathic T1D patients showed an older onset age, higher body mass index among adults, lower haemoglobin A1c, higher levels of fasting C‐peptide and 2‐h postprandial C‐peptide, and were likely to have type 2 diabetes (T2D) family history and carry 0 susceptible HLA haplotype (all p < 0.01). A lower proportion of individuals carrying 2 susceptible HLA haplotypes in idiopathic T1D was observed in the adult‐onset subgroup (15.7% vs. 38.0% in child‐onset subgroup, p < 0.001) and in subgroup with preserved beta‐cell function (11.0% vs. 30.1% in subgroup with poor beta‐cell function, p < 0.001). Multivariable correlation analyses indicated that being overweight, having T2D family history and lacking susceptible HLA haplotypes were associated with negative autoantibodies. Conclusions: Idiopathic T1D represents about 1/4 of newly diagnosed T1D, with adult‐onset and preserved beta‐cell function patients showing lower HLA susceptibility and more insulin resistance. [ABSTRACT FROM AUTHOR]

Aims: This study investigated insulinoma‐associated‐2 autoantibody (IA‐2A) and zinc transporter 8 autoantibody (ZnT8A) distribution in patients with type 1 diabetes (T1D) and latent autoimmune diabetes (LAD) and the autoantibodies' association with clinical characteristics and HLA‐DR‐DQ genes. Materials and Methods: This cross‐sectional study recruited 17,536 patients with diabetes from 46 hospitals across China. A total of 189 patients with T1D and 58 patients with LAD with IA‐2A positivity, 126 patients with T1D and 86 patients with LAD with ZnT8A positivity, and 231 patients with type 2 diabetes (T2D) were selected to evaluate islet autoantibodies, clinical phenotypes, and HLA‐DR‐DQ gene frequency. Results: IA‐2A was bimodally distributed in patients with T1D and LAD. Patients with low IA‐2A titre LAD had lower fasting C‐peptide (FCP) (p < 0.01), lower postprandial C‐peptide (PCP) (p < 0.001), and higher haemoglobin A1c (HbA1c) levels (p < 0.05) than patients with T2D. Patients with high IA‐2A titre LAD were younger than patients with low IA‐2A titre LAD (p < 0.05). Patients with low IA‐2A titre T1D had lower FCP (p < 0.01), lower PCP (p < 0.01), and higher HbA1c levels (p < 0.05) than patients with high IA‐2A titre LAD. HLA‐DR‐DQ genetic analysis demonstrated that the frequency of susceptible HLA haplotypes was higher in IA‐2A‐positive patients (p < 0.001) than in patients with T2D. Patients with high ZnT8A titre LAD had lower FCP (p = 0.045), lower PCP (p = 0.023), and higher HbA1c levels (p = 0.009) and a higher frequency of total susceptible haplotypes (p < 0.001) than patients with low ZnT8A titre LAD. Conclusions: IA‐2A in patients with T1D and LAD was bimodally distributed, and the presence of IA‐2A could demonstrate partial LAD clinical characteristics. ZnT8A titre had a certain predictive value for islet functions in patients with LAD. [ABSTRACT FROM AUTHOR]

Aim: To investigate the impact of family history of type 2 diabetes (T2D) on the clinical phenotypes of patients with idiopathic type 1 diabetes (T1D). Methods: In clinically diagnosed T1D cases, a total of 335 idopathic T1D patients were included in the study, after excluding autoimmune T1D using islet autoantibody testing and monogenic diabetes using a custom monogenic diabetes gene panel obtained from clinically diagnosed T1D cases. A semi‐structured questionnaire was used to collect information on the presence of T2D in first‐degree relatives. The demographic and metabolic markers of idiopathic T1D patients were analysed. Subgroup analysis was performed to investigate potential interactions between T2D family history and human leukocyte antigen (HLA) genotypes. Results: A total of 18.2% of individuals with idiopathic T1D had a T2D family history, and these individuals were more likely to have features associated with T2D, such as older age of onset, higher body mass index at diagnosis, lower insulin dosage and better beta‐cell function, as indicated by higher levels of fasting C‐peptide and 2‐hour postprandial C‐peptide (all P < 0.05). Additionally, regardless of HLA susceptible genotypes, the impact of family history of T2D was consistently observed in idiopathic T1D patients. Multivariable analyses showed that T2D family history was negatively correlated with the risk of beta‐cell function failure in idiopathic T1D patients (P < 0.05). Conclusions: Family history of T2D may be implicated in the heterogeneity of idiopathic T1D patients. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is a complex autoimmune disease characterized by an absolute deficiency of insulin. It affects more than 20 million people worldwide and imposes an enormous financial burden on patients. The underlying pathogenic mechanisms of T1D are still obscure, but it is widely accepted that both genetics and the environment play an important role in its onset and development. Previous studies have identified more than 60 susceptible loci associated with T1D, explaining approximately 80%‐85% of the heritability. However, most identified variants confer only small increases in risk, which restricts their potential clinical application. In addition, there is still a so‐called 'missing heritability' phenomenon. While the gap between known heritability and true heritability in T1D is small compared with that in other complex traits and disorders, further elucidation of T1D genetics has the potential to bring novel insights into its aetiology and provide new therapeutic targets. Many hypotheses have been proposed to explain the missing heritability, including variants remaining to be found (variants with small effect sizes, rare variants and structural variants) and interactions (gene–gene and gene–environment interactions; e.g. epigenetic effects). In the following review, we introduce the possible sources of missing heritability and discuss the existing related knowledge in the context of T1D. [ABSTRACT FROM AUTHOR]

Aims and Objectives: Fulminant type 1 diabetes (FT1D) could present diabetes ketoacidosis (DKA) at early onset. It is crucial to identify FT1D from DKA manifestations in time at clinical practice. This study was aimed at investigating whether the fulminant index (FI), encompassing plasma glucose (PG) to glycated haemoglobin (HbA1c) ratio (PG/HbA1c), serum potassium ion (K+) to HbA1c ratio (K+/HbA1c) and serum sodium ion (Na+) multiplied by HbA1c (Na+*HbA1c), is a feasible indicator for early FT1D diagnosis. Materials and Methods: A total of 78 subjects were enroled, including 40 FT1D patients and 38 non‐FT1D patients with DKA. We utilised receiver operating characteristic (ROC) curve analysis to determine the FI cut‐off values between FT1D and non‐FT1D groups and examined efficacies of FI based on statistics. Results: ROC curve analyses showed that the maximum Youden's index for PG/HbA1c bonding to a cut‐off value of 4.389, with the sensitivity of 75.0% and specificity of 81.6% in identifying FT1D from DKA. And optimal K+/HbA1c cut‐off value was 0.728 with a sensitivity of 90.0% and specificity of 84.2%. For Na+*HbA1c, the best cut‐off value was 923.65, and its sensitivity and specificity were 85% and 73.7%, respectively. Conclusions: These results suggested FI could work as a valid and convenient indicator for differentiating FT1D from initial DKA patients. FI (K+/HbA1c) presented the best efficacy as an independent index. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to establish a systematic screening strategy to select candidates for genetic testing among patients with maturity‐onset diabetes of the young (MODY) and to accomplish early diagnosis of MODY. Materials and methods: We enrolled 1478 sporadic patients from the outpatient department of endocrinology. Out of the1478 patients, 1279 participants were successfully screened according to the "AACM" strategy, which includes the age of onset, autoantibody to islet antigen, C‐peptide and metabolic syndrome. Another six probands and their families who fulfilled the common clinical criteria for MODY were also examined for causative gene mutations. Whole‐exome sequencing (WES) was performed to examine the mutations. Results: A total of 24 out of 1279 sporadic patients with newly diagnosed diabetes were eligible for genetic testing. Mutations were found in 4/24 participants in the cohort, as well as in 2/6 pedigrees. A likely pathogenic alteration, a likely benign alteration and three alterations with uncertain significance were identified with WES. Most of the mutant genes recognised in our trial were not the most common causative genes of MODY, and all of the mutations were specifically reported in Asian patients only, suggesting a unique genetic background of MODY in different ethnicities. Conclusions: In this systematic study of MODY in a new‐onset diabetes cohort, MODY cases were incorrectly diagnosed as type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM), suggesting that an observant clinician is necessary for early and correct MODY diagnosis. This systematic approach to screening is practical and specific enough to identify patients who are most appropriate for genetic testing. [ABSTRACT FROM AUTHOR]

Aim: To investigate the frequency, clinical phenotype, inflammatory cytokine levels and genetics of glutamic acid decarboxylase autoantibody (GADA)‐positive phenotypic youth‐onset type 2 diabetes. Materials and Methods: This nationwide, multicentre, cross‐sectional study included 5324 newly diagnosed subjects with phenotypic type 2 diabetes aged 15 years or older enrolled in the LADA China study. GADA was screened in 248 subjects with youth‐onset type 2 diabetes aged 15–29 years. Subjects who presented as GADA‐positive were defined as having latent autoimmune diabetes in youth (LADY). We added subjects with LADY, type 1 diabetes, type 2 diabetes and controls from the Diabetes Center of Central South University, and measured serum concentrations of interleukin‐6, lipocalin 2, high‐sensitivity C‐reactive protein, adiponectin and human leukocyte antigen (HLA) genotyping in subjects with LADY, age‐ and sex‐matched GADA‐negative type 2 diabetes, type 1 diabetes and controls. Results: Twenty‐nine of the 248 subjects (11.7%) were GADA positive. Compared with subjects with type 2 diabetes, subjects with LADY were less probable to have metabolic syndrome (27.6% vs. 59.4%; p =.001). The fasting C‐peptide levels tended to be lower in subjects with LADY than in subjects with type 2 diabetes, but the difference was not statistically significant (LADY vs. type 2 diabetes: 0.21 [0.17–0.64] vs. 0.47 [0.29–0.77] nmol/L; p =.11). The cytokine levels of subjects with LADY were indistinguishable from subjects with type 1 diabetes, but subjects with LADY presented increased adiponectin levels compared with subjects with type 2 diabetes after adjusting for age, sex and body mass index (7.19 [4.05–11.66] vs. 3.42 [2.35–5.74] μg/mL; p <.05). The frequency of total susceptible HLA genotypes (DR3/3, −3/9 and −9/9) in subjects with LADY and type 1 diabetes were similarly higher than controls (LADY and type 1 diabetes vs. controls: 21.4% and 30.8% vs. 2.6%, respectively; p <.001). Conclusions: A high GADA positivity was observed in youth‐onset type 2 diabetes subjects in China. As subjects with LADY had an increased susceptible HLA genetic load and different cytokine levels compared with subjects with type 2 diabetes, differentiating LADY from phenotypic type 2 diabetes subjects is important. [ABSTRACT FROM AUTHOR]

Aims: Circular RNAs (circRNAs) have recently been shown to exert important effects in human diseases. However, the roles of circRNAs in type 1 diabetes (T1D) are largely unknown. This study is to identify the circRNA expression profiles in the peripheral blood of patients with T1D and predict their potential regulatory mechanisms and coding potential. Methods: CircRNA expression profiles were detected by Arraystar human circRNA microarray. With real‐time PCR validation, multiple bioinformatics approaches were used to explore their biological functions, construct the circRNA‐miRNA‐mRNA interactions, and predict circRNA coding potential. Results: A total of 93 differentially expressed circular transcripts were identified in T1D compared with controls, among which 30 were upregulated, and 63 were downregulated. Two circRNAs were identified to have significant differences by RT‐PCR. Gene ontology analysis enriched terms such as cellular protein metabolic process, cytoplasm and zinc ion binding. The proposed molecular functions of these differentially expressed circRNAs, including cellular protein metabolic process, cytoplasm, and binding, may contribute to T1D. The most enriched pathways for these circRNAs were involved in protein processing in the endoplasmic reticulum. Hsa_circ_0072697 may be involved in 50 circRNA‐miRNA‐mRNA signalling pathways related to diabetes, such as circ_0072697‐miR‐15a‐UBASH3A network. Furthermore, hsa_circ_0071224, hsa_circ_0002437, hsa_circ_0084429, hsa_circ_0072697, and hsa_circ_0000787 in T1D were considered to have the most coding potential involved in the pathogenesis of T1D. Conclusions: These results showed that circRNAs are aberrantly expressed in the peripheral blood of patients with T1D and may play potential actions by interactions with miRNA and circRNA‐derived peptides in the development of T1D. [ABSTRACT FROM AUTHOR]

Fulminant type 1 diabetes (FT1D) is a subset of type 1 diabetes characterized by extremely rapid pancreatic β-cell destruction with aggressive progression of hyperglycaemia and ketoacidosis. It was initially classified as idiopathic type 1 diabetes due to the absence of autoimmune markers. However, subsequent studies provide evidences supporting the involvement of autoimmunity in rapid β-cell loss in FT1D pathogenesis, which are crucial for FT1D being an autoimmune disease. This article highlights the role of immunological aspects in FT1D according to the autoimmune-associated genetic background, viral infection, innate immunity, adaptive immunity, and pancreas histology. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Genetic and epigenetic mechanisms have been implicated in the pathogenesis of type 1 diabetes, and histone acetylation is an epigenetic modification pattern that activates gene transcription. However, the genome‐wide histone H3 acetylation in new‐onset type 1 diabetes patients has not been well described. Accordingly, we aimed to unveil the genome‐wide promoter acetylation profile in CD4+ T lymphocytes from type 1 diabetes patients, especially for those who are glutamate decarboxylase antibody‐positive. Materials and Methods: A total of 12 patients with new‐onset type 1 diabetes who were glutamate decarboxylase antibody‐positive were enrolled, and 12 healthy individuals were recruited as controls. The global histone H3 acetylation level of CD4+ T lymphocytes from peripheral blood was detected by western blot, with chromatin immunoprecipitation linked to microarrays to characterize the promoter acetylation profile. Furthermore, we validated the results of particular genes from chromatin immunoprecipitation linked to microarrays by using chromatin immunoprecipitation quantitative polymerase chain reaction, and analyzed the transcription level by real‐time quantitative polymerase chain reaction. Results: Elevated global histone H3 acetylation level was observed in type 1 diabetes patients, with 607 differentially acetylated genes identified between type 1 diabetes patients and controls by chromatin immunoprecipitation linked to microarrays. The hyperacetylated genes were enriched in biological processes involved in immune cell activation and inflammatory response. Gene‐specific assessments showed that increased transcription of inducible T‐cell costimulator was in concordance with the elevated acetylation in its gene promoter, along with positive correlation with glutamate decarboxylase antibody titer in type 1 diabetes patients. Conclusions: The present study generates a genome‐wide histone acetylation profile specific to CD4+ T lymphocytes in type 1 diabetes patients who are glutamic acid decarboxylase antibody‐positive, which is instrumental in improving our understanding of the epigenetic involvement in autoimmune diabetes. Patients with type 1 diabetes displays a distinct histone H3 acetylation profile in gene promoters in CD4+ T lymphocytes. Elevated histone H3 acetylation is associated with genes involving in T lymphocyte activation. GAD antibody production in T1D patients was associated with the hyperacetylation and increased expression of co‐stimulator ICOS. [ABSTRACT FROM AUTHOR]

HighlightsThis study reports a novel frameshift mutation c.212dupG (p.Gly73fs) in the insulin (INS) gene causing maturity onset diabetes of the young (MODY) 10, one of the rare types of MODY, identified in seven family members.Screening for mutations in identified MODY genes is warranted in patients who require insulin, are negative for autoantibodies but have a family history of diabetes. [ABSTRACT FROM AUTHOR]

Abstract: There is a morpheme tu ‘know’ in Acehnese (Malayo‐Polynesian) that always needs to combine with so‐called epistemological classifiers specifying conceptual categories of knowledge. On the empirical side, this paper reports first‐hand data involving tu combined with epistemological classifiers. The primary purpose is to demonstrate what epistemological classifiers combine with tu, when tu takes a declarative clause, an overt wh‐clause, or a DP that receives an interrogative reading (“concealed questions”). When tu takes a declarative clause, the epistemological classifier combined with it invariably is peue ‘what.’ When tu takes an overt wh‐clause, the epistemological classifier is either the default peue ‘what’ or the same as the (surface highest) epistemological classifier in the wh‐clause. When tu embeds a concealed question DP, the epistemological classifier is morphologically sensitive to what question the DP is intended to express. The theoretical component of this paper mainly focuses on tu embedding concealed question DPs. I argue that Acehnese concealed questions are best analyzed as wh‐questions in disguise, from which the wh‐word is ellipticized at the PF level. Researchers have previously argued that the question‐in‐disguise analysis of concealed questions does not work for concealed questions in such languages as English and Spanish. Hence, the discussion of concealed questions in Acehnese suggests that the interpretation of concealed questions may show interesting and important crosslinguistic variability. [ABSTRACT FROM AUTHOR]

Background: Latent autoimmune diabetes in adults (LADA) is a form of autoimmune diabetes with heterogeneous features. This study aimed to investigate the persistent status of glutamic acid decarboxylase antibody (GADA) in patients with LADA and its association with clinical characteristics.Methods: This 3-year follow-up study enrolled 107 LADA and 40 type 2 diabetes mellitus (T2DM) patients from October 2005 to December 2013. GADA titer, epitopes, and clinical characteristics (including fasting C-peptide and HbA1c ) in LADA patients were assayed annually. The human leukocyte antigen DQ (HLA-DQ) genotypes were also analysed. The relationship between the persistence of GADA and the clinical characteristics was investigated in LADA patients.Results: After 3-year follow-up, 36.5% (39/107) LADA patients remained GADA positive (persistently positive group), 19.6% (21/107) patients fluctuated positively and negatively (fluctuating group), and 43.9% (47/107) patients became GADA negative, among which 61.7% (29/47) seroconversions occurred within 6 months of follow-up (transiently positive group). The GADA persistently positive group possessed higher titer of GADA than transiently positive group and fluctuant group (all p = 0.000), higher reactivities to middle and C-terminal regions of GAD65 than those in transiently positive group (p = 0.001 and p = 0.000, respectively), and lower baseline fasting C-peptide level than T2DM patients and transiently positive group [415(31-1862) vs 620(220-1658) pmol/L, p = 0.014; and 415(31-1862) vs 705(64-1541) pmol/L, p = 0.017, respectively]. The GADA transiently positive group retained a higher HbA1c level when compared with T2DM patients (p = 0.023). In addition, the three LADA groups shared similar frequencies of HLA-DQ susceptible haplotypes that were higher as compared with T2DM. The GADA persistently positive group had a higher annual declining rate in fasting C-peptide than T2DM patients [-14%(-174-33%) vs -1%(-27-28%), p = 0.007].Conclusion: The LADA patients with GADA transient positivity account for a large proportion, whose clinical characteristics and HLA-DQ haplotypes are different from those of T2DM. The patients with high titer GADA and reactivities to GADA65 middle and C-terminal regions showed a persistent GADA positivity, in which a worse baseline and accelerated decline of β-cell function need early intervention in the practice. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 58-year-old Chinese woman with type 2 diabetes and severe diabetic ketoacidosis (DKA) due to insulin antibodies. Topics discussed include the administration of insulin therapy to the patient, the measurement of the insulin antibody before and after treatment, and the assessment of insulin demand, glycemic control, titers and competitive inhibition assay for antibodies.

The article presents a long-term study on hydrolytic degradation and morphology of poly(ethylene glycol terephthalate)-b-poly(butylene terephthalate) (PEGT-b-PBT) copolymer films. It found that hydrolytic degradation profiles of PEGT-b-PBT polymer films at 37°C in phosphate-buffered saline (PBS) in a period of 300 days rely on copolymer composition and degradable time. It adds that films with higher PEGT content exhibit a faster decrease in intrinsic viscosity and mass loss.

Background: There are abundant variations in the phenotypes and genetics of type 1 diabetes (T1D) patients across different races. This study aimed to assess differences between juvenile acute onset (JAO) and adult acute onset in Chinese T1D patients.Methods: Seven hundred and fifty-one acute onset T1D patients were divided into two groups by the patient onset age as follows: the juvenile acute onset group (≤20 years, JAO group) and the adult acute onset group (>20 years, AAO group). Clinical characteristics, islet autoantibodies, and HLA class II haplotypes and genotypes were compared between these two groups.Results: In comparison with AAO patients, JAO patients had significantly lower relative weights and lower triglyceride levels (P < .001, P < .01, respectively) but higher frequency of ketoacidosis (P < .001), higher daily insulin dosage (Pc  < .001), higher HbA1c (Pc  < .05), and higher HDL-cholesterol levels (Pc  < .01). The JAO group showed a higher prevalence of IA-2A, ZnT8A, and multiple autoantibodies than that in the AAO group (P < .001, P < .01, P < .001, respectively). Haplotypes for DRB1*0301-DQA1*03-DQB1*0201, DR3, DR4, DR9, and DR3/DR9 genotypes are highly associated with JAO susceptibility, whereas only DR3 and DR9 genotypes confer risk for AAO. In the JAO group but not the AAO group, DR3 is related to ZnT8A, and DR3/DR9 is related to IA-2A and multiple autoantibodies.Conclusions: These observations suggest that JAO patients markedly differ from AAO patients in their clinical manifestations and genetics in the Chinese T1D population. Notably, the DR3/DR9 genotype can facilitate the appearance of IA-2A or multiple autoantibodies in JAO patients. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 51-year-old Chinese woman who was receiving peginterferon α-2a therapy for hepatitis C for a year and was diagnosed with severe diabetic ketoacidosis and FTID (Fulminant type 1 diabetes) at the time of admission. It notes FTID is caused by peginterferon treatment and the patient is positive for glutamic acid decarboxylase autoantibody (GADA) and the patient was treated by withdrawing peginterferon.

Background: Latent autoimmune diabetes in adults (LADA) exhibits significant clinical heterogeneity, but the underlying causes remain unclear. The aim of this study was to investigate whether age of onset of LADA contributes to the observed clinical heterogeneity by comparing the clinical, metabolic, and immunogenetic characteristics between elderly and young LADA patients.Methods: The cross-sectional study included a total of 579 patients with LADA which was further divided into elderly LADA (E-LADA) group (n = 135, age of onset ≥60 years) and young LADA (Y-LADA) group (n = 444, age of onset <60 years). Age-matched subjects with type 2 diabetes were served as control (E-T2D group, n = 622). Clinical characteristics, serum autoantibodies, and HLA-DQ haplotypes were compared among these groups.Results: Compared with patients with Y-LADA, patients with E-LADA have better residual beta-cell function and higher level of insulin resistance (both P < .01), more metabolic syndrome characteristics, similar proportion of islet autoantibody positivity, and strikingly different HLA-DQ genetic background. In comparison with E-T2D patients, E-LADA patients tend to have similar metabolic syndrome prevalence, comparable C-peptide levels, and insulin resistance levels and share similar HLA-DQ genetic characteristics.Conclusions: Elderly LADA differs phenotypically and genetically from Y-LADA but has a clinical and genetic profile more similar to that of E-T2D. These distinct phenotypes could potentially help physicians better manage patients with E-LADA. [ABSTRACT FROM AUTHOR]

A wealth of epidemiological studies concerning the distribution of type 1 diabetes (T1D) around the world have pointed to the appreciable variation in the incidence of T1D among disparate age groups, ethnicities, and geographical locations. On the whole, the incidence of childhood T1D has been on the rise, and a plausible inverse relationship between the initial incidence rate and the following annual increase in incidence has been raised. Countries that used to exhibit lower incidences tend to have steep annual increase whereas those with already-established high incidences are more likely to show a modest increase or even stabilization in T1D incidence. Environmental agents considered responsible for the current evolving pattern of T1D incidence will be detailed, mainly including the increasing prevalence of childhood obesity, viral infections in a chronic manner, maternal-child interaction such as breastfeeding, and latitude-ultraviolet B-vitamin D pathway. Certain rationale has been put forward in an attempt to explain the potential association between environmental agents and development of T1D. For instance, accelerator hypothesis regards insulin resistance as the promoter of earlier disease onset in obese children whereas the negative correlation of microbial infections in background populations with incidence of T1D represents the basic component of the hygiene hypothesis. Further investigations are still warranted to verify these theories across multiple ethnic groups and to identify additional contributors to the variation in T1D incidence. [ABSTRACT FROM AUTHOR]