Endodontic considerations of survival rate for autotransplanted third molars: a nationwide population-based study.

AIM: To investigate whether the timing of root canal treatment (primary aim) or other endodontic parameters (secondary aim) is associated with the survival probability of autotransplanted third molars, using a nationwide population-based database. METHODOLOGY: A total of 1811 third molars autotransplanted between 2000 and 2013 met the inclusion criteria and were followed until the end of 2016. The teeth were classified into three groups on the basis of timing between root canal treatment and the autotransplantation: preoperative, extraoral and postoperative treatment groups. Univariate and multivariate Cox proportional hazards models were used to estimate the association between the timing of root canal treatment and the risk of tooth extraction after autotransplantation. RESULTS: Of the 1811 autotransplanted third molars, 462 were extracted, yielding a 17-year survival probability of 0.578. The survival probability of autotransplanted teeth that received postoperative root fillings after 17 years was 0.583, which was significantly higher than the 0.434 and 0.566 for teeth that received preoperative and extraoral root fillings, respectively (P = 0.0013). After adjustment for potential confounding factors, teeth that received postoperative root fillings were associated with a significantly lower tooth extraction hazard ratio (HR) compared with those that received extraoral root fillings (adjusted HR, 1.43; 95% confidence interval [CI], 1.14-1.78) and those that received preoperative root fillings (adjusted HR, 2.13; 95% CI, 1.19-3.82). Furthermore, the use of a rubber dam during postoperative root filling was associated with a significantly lower extraction rate after autotransplantation (adjusted HR, 0.54; 95% CI, 0.43-0.69). CONCLUSIONS: Postoperative root canal treatment resulted in a significantly lower extraction rate than did preoperative or extraoral root canal treatment amongst autotransplanted third molars during a mean follow-up period of 8.33 years. Rubber dam use is recommended during postoperative root canal treatment to improve the outcomes of autotransplantation.

The roles of autophagy and hypoxia in human inflammatory periapical lesions.

AIM: To determine the expressions of hypoxia-related [hypoxia-inducible transcription factors (HIF)-1α, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) and phospho-adenosine monophosphate activated protein kinase (pAMPK)] and autophagy-related [microtubule-associated protein 1 light chain 3 (LC3), beclin-1 (BECN-1), autophagy-related gene (Atg)5-12, and p62] proteins in human inflammatory periapical lesions. METHODOLOGY: Fifteen samples of radicular cysts (RCs) and 21 periapical granulomas (PGs), combined with 17 healthy dental pulp tissues, were examined. Enzyme-linked immunosorbent assay (ELISA) was used to detect interleukin (IL)-1ß cytokine; immunohistochemical (IHC) and Western blot (WB) analyses were employed to examine autophagy-related and hypoxia-related proteins. Transmission electron microscopy (TEM) was used to explore the ultrastructural morphology of autophagy in periapical lesions. Nonparametric Kruskal-Wallis tests and Mann-Whitney U-tests were used for statistical analyses. RESULTS: ELISA revealed a significantly higher (P < 0.001) IL-1ß expression in periapical lesions than in normal pulp tissue. Immunoscores of IHC expressions of pAMPK, HIF-1α, BNIP3, BECN-1 and Atg5-12 proteins in periapical lesions were significantly higher (P < 0.001) (except BECN-1) than those in normal pulp tissue. The results of IHC studies were largely compatible with those of WB analyses, where significantly higher (P < 0.05) expressions of hypoxia-related and autophagy-related proteins (except BECN-1, p62 and LC3II in WB analyses) in periapical lesions were noted as compared to normal pulp tissue. Upon TEM, ultrastructural double-membrane autophagosomes and autolysosomes were observed in PGs and RCs. CONCLUSIONS: Autophagy associated with hypoxia may play a potential causative role in the development and maintenance of inflamed periapical lesions.

Depression and physical health multimorbidity: primary data and country-wide meta-analysis of population data from 190 593 people across 43 low- and middle-income countries.

BACKGROUND: Despite the known heightened risk and burden of various somatic diseases in people with depression, very little is known about physical health multimorbidity (i.e. two or more physical health co-morbidities) in individuals with depression. This study explored physical health multimorbidity in people with clinical depression, subsyndromal depression and brief depressive episode across 43 low- and middle-income countries (LMICs). METHOD: Cross-sectional, community-based data on 190 593 individuals from 43 LMICs recruited via the World Health Survey were analysed. Multivariable logistic regression analysis was done to assess the association between depression and physical multimorbidity. RESULTS: Overall, two, three and four or more physical health conditions were present in 7.4, 2.4 and 0.9% of non-depressive individuals compared with 17.7, 9.1 and 4.9% among people with any depressive episode, respectively. Compared with those with no depression, subsyndromal depression, brief depressive episode and depressive episode were significantly associated with 2.62, 2.14 and 3.44 times higher odds for multimorbidity, respectively. A significant positive association between multimorbidity and any depression was observed across 42 of the 43 countries, with particularly high odds ratios (ORs) in China (OR 8.84), Laos (OR 5.08), Ethiopia (OR 4.99), the Philippines (OR 4.81) and Malaysia (OR 4.58). The pooled OR for multimorbidity and depression estimated by meta-analysis across 43 countries was 3.26 (95% confident interval 2.98-3.57). CONCLUSIONS: Our large multinational study demonstrates that physical health multimorbidity is increased across the depression spectrum. Public health interventions are required to address this global health problem.

Rapidly increasing liver progenitor cell numbers in human regenerating liver after portal vein ligation and liver partition.

BACKGROUND: Liver regeneration is dependent on the proliferation of hepatocytes. Hepatic progenitor cells are intra-hepatic precursor cells capable of differentiating into hepatocytes or biliary cells. Although liver progenitor cell proliferation during the regenerative process has been observed in animal models of severe liver injury, it has never been observed in vivo in humans because it is unethical to take multiple biopsy specimens for the purpose of studying the proliferation of liver progenitor cells and the roles they play in liver regeneration. Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) is a staged procedure for inducing remnant liver hypertrophy so that major hepatectomy can be performed safely. This staged procedure allows for liver biopsy specimens to be taken before and after the liver begins to regenerate. CASE PRESENTATION: The liver progenitor cell proliferation is observed in a patient undergoing ALPPS for a metastatic hepatic tumour. Liver biopsy is acquired before and after ALPPS for the calculation of average number of liver progenitor cell under high magnification examination by stain of immunomarkers. This is the first in vivo evidence of growing liver progenitor cells demonstrated in a regenerating human liver.

A novel HLA-A*02 variant, HLA-A*02:575, detected in a Taiwanese bone marrow hematopoietic stem cell donor.

One nucleotide substitution at residue 410 of HLA-A*02:07:01 results in a new allele, HLA-A*02:575.

HLA-DRB1*14:84 may have been derived from HLA-DRB1*14:05 and HLA-DRB1*04:58 via a genetic recombination event.

Derivation of HLA-DRB1*14:84 via a genetic recombination event.

Detection of a novel variant of HLA-B*07, HLA-B*07:249, in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide replacement at residue 398 of HLA-B*07:05:01 or HLA-B*07:06 results in a novel allele, HLA-B*07:249.

Detection of a novel variant of HLA-A*02, HLA-A*02:570, in a Taiwanese unrelated hematopoietic stem cell donor.

Two nucleotide changes at residue 142 (G → A) and residue 144 (A → C) of HLA-A*02:01:01:01 result in a novel allele, HLA-A*02:570.

A novel human leukocyte antigen (HLA) allele, HLA-DRB1*08:71, was found in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide substitution at residue 367 of HLA-DRB1*08:03:02 results in a new allele, HLA-DRB1*08:71.

A single nucleotide replacement in exon 2 produces a novel HLA-C*01:02 variant, HLA-C*01:02:34.

HLA-C*01:02:34 differs from HLA-C*01:02:01 by a single nucleotide replacement in codon 43.

Detection of a novel HLA-B*15 variant, HLA-B*15:01:37, in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide substitution at residue 531 of HLA-B*15:01:01:01 results in a new allele, HLA-B*15:01:37.

Identification of a novel HLA-B*46:01 variant, HLA-B*46:01:20, in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide replacement at residue 528 of HLA-B*46:01:01 results in a new allele, HLA-B*46:01:20.

The novel HLA-DRB1*12:01:06 allele detected in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide substitution at residue 267 of HLA-DRB1*12:01:01 results in a new allele, HLA-DRB1*12:01:06.

A novel HLA allele, HLA-DRB1*15:116, discovered in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide substitution at residue 127 of HLA-DRB1*15:01:01:01 results in a new allele, HLA-DRB1*15:116.

HLA-A*24:287, a novel variant of HLA-A*24:02:01:01, discovered in a Taiwanese hematopoietic stem cell donor.

One nucleotide replacement in codon 182 of HLA-A*24:02:01:01 results in a novel allele, HLA-A*24:287.

HLA-B*46:60, a novel variant of HLA-B*46:01:01, detected in a Taiwanese unrelated hematopoietic stem cell donor by sequence-based typing.

One nucleotide replacement at residue 89 of HLA-B*46:01:01 results in a novel allele, HLA-B*46:60.

HLA-B*15:327, a novel variant of HLA-B*15, discovered in a Taiwanese unrelated hematopoietic stem cell donor.

One nucleotide substitution at residue 86 of HLA-B*15:27:01 results in a new allele, HLA-B*15:327.

HLA-A*02:541, a novel variant of HLA-A*02, discovered in a Taiwanese unrelated hematopoietic stem cell donor.

Two nucleotide changes at residue 524 and residue 527 of HLA-A*02:07:01 results in a novel allele, HLA-A*02:541.

A single nucleotide deletion in exon 3 of the HLA-C*07:02:01:01 allele produces a novel HLA-C*07 null allele, HLA-C*07:393N.

A single nucleotide deletion in HLA-C*07:02:01:01 results in a novel null allele, HLA-C*07:393N.

Identification of a novel HLA-DRB1*04 null allele, HLA-DRB1*04:178N.

A single nucleotide insertion in codon 77 of HLA-DRB*04:05:01 results in a null allele, HLA-DRB1*04:178N.