Severe Acute Hepatitis Outbreaks Associated with a Novel Hepacivirus in Rhizomys pruinosus in Hainan, China.

Members of the genus Hepacivirus have a broad range of hosts, with at least 14 species identified. To date, a highly pathogenic hepacivirus causing severe disease in animals has not been found. Here, by using high-throughput sequencing, a new hepacivirus was identified as the dominant and highly pathogenic virus in severe acute hepatitis outbreaks in bamboo rats (Rhizomys pruinosus), with ≈80% mortality; this virus emerged in February 2020 in two bamboo rat farms in China. Hepaciviral genome copies in bamboo rat liver were significantly higher than in other organs. Genomic sequences of hepacivirus strains from 12 sick bamboo rats were found to share 85.3 to 100% nucleotide (nt) identity and 94.9 to 100% amino acid (aa) identity and to share 79.7 to 87.8% nt and 90.4 to 97.8% aa identities with previously reported bamboo rat hepaciviruses of Vietnam and China. Sequence analysis further revealed the simultaneous circulation of genetically divergent hepacivirus variants within the two outbreaks. Phylogenetic analysis showed that hepacivirus strains from the present and previous studies formed an independent clade comprised of at least two genotypes, clearly different from all other known species, suggesting a novel species within the genus Hepacivirus. This is the first report of a non-human-infecting hepacivirus causing potentially fatal infection of bamboo rats, and the associated hepatitis in the animals potentially can be used to develop a surrogate model for the study of hepatitis C virus infection in humans and for the development of therapeutic strategies. IMPORTANCE Members of the genus Hepacivirus have a broad host range, with at least 14 species identified, but none is highly pathogenic to its host except for hepatitis C virus, which causes severe liver diseases in humans. In this study, a new liver-tropic hepacivirus species was identified by high-throughput sequencing as the pathogen associated with two outbreaks of severely acute hepatitis in hoary bamboo rats (Rhizomys pruinosus) on two farms in Hainan Province, China; this is the first reported highly pathogenic animal hepacivirus to our knowledge. Further phylogenetic analysis suggested that the hepaciviruses derived from hoary bamboo rats in either the current or previous studies represent a novel species within the genus Hepacivirus. This finding is a breakthrough that has significantly updated our understanding about the pathogenicity of animal hepaciviruses, and the hepacivirus-associated hepatitis in bamboo rats may have a use as an animal infection model to understand HCV infection and develop therapeutic strategies.

Peripheral artery disease independently associated with significantly higher risk for COVID-19 mortality: Evidence based on adjusted effect estimates.

OBJECTIVE: To investigate the influence of peripheral artery disease (PAD) on the risk of mortality among coronavirus disease 2019 (COVID-19) patients based on adjusted effect estimates. METHODS: Systematic searches were performed through electronic databases. A random-effect model was applied to calculate the pooled effect and corresponding 95% confidence interval (CI). Inconsistency index (I2) was used to evaluate the heterogeneity across studies. Sensitivity analysis, subgroup analysis, and Begg's test were all implemented. RESULTS: On the basis of 16 eligible studies with 142,832 COVID-19 patients, the meta-analysis showed that PAD significantly increased the risk for mortality among COVID-19 patients (pooled effect = 1.29, 95% CI: 1.10-1.51). The significant association was also observed in the subgroup analysis stratified by hospitalized patients, mean age ≥ 60 years, Europe and North America. Sensitivity analysis verified the robustness of our findings. Begg's test (P = 0.15) showed there was no potential publication bias. CONCLUSIONS: COVID-19 patients with PAD may have a greater risk of mortality. Clinicians and nursing staff are supposed to identify and monitor these high-risk patients in a timely manner and provide appropriate clinical treatment for them.

Significant association between anemia and higher risk for COVID-19 mortality: A meta-analysis of adjusted effect estimates.

OBJECTIVE: This study aimed to evaluate whether there was a significant relationship between anemia and the risk for mortality among coronavirus disease 2019 (COVID-19) patients by a quantitative meta-analysis based on the adjusted effect estimates. METHODS: A systematic search was conducted in electronic databases to identify all published literature. A random-effects meta-analysis model was used to estimate the pooled effect size and 95% confidence interval (CI). Heterogeneity test, Begg's test, subgroup analysis and meta-regression were performed. RESULTS: Twenty-three articles with 573,928 COVID-19 patients were included in the quantitative meta-analysis. There was a significant association between anemia and an elevated risk of COVID-19 mortality (pooled effect size = 1.47, 95% CI [1.30-1.67]). We observed this significant association in the further subgroup analyses by age, proportion of males, sample size, study design, region and setting. Sensitivity analysis exhibited that our results were reliable. Begg's test showed that there was no publication bias. Meta-regression indicated that the tested variables might not be the source of heterogeneity. CONCLUSION: Our meta-analysis based on risk factors-adjusted effect estimates indicated that anemia was independently associated with a significantly elevated risk for mortality among COVID-19 patients.

Systematic analysis reveals a functional role for STAMBPL1 in the epithelial-mesenchymal transition process across multiple carcinomas.

BACKGROUND: Deubiquitinating enzymes (DUBs) are linked to cancer progression and dissemination, yet less is known about their regulation and impact on epithelial-mesenchymal transition (EMT). METHODS: An integrative translational approach combining systematic computational analyses of The Cancer Genome Atlas cancer cohorts with CRISPR genetics, biochemistry and immunohistochemistry methodologies to identify and assess the role of human DUBs in EMT. RESULTS: We identify a previously undiscovered biological function of STAM-binding protein like 1 (STAMBPL1) deubiquitinase in the EMT process in lung and breast carcinomas. We show that STAMBPL1 expression can be regulated by mutant p53 and that its catalytic activity is required to affect the transcription factor SNAI1. Accordingly, genetic depletion and CRISPR-mediated gene knockout of STAMBPL1 leads to marked recovery of epithelial markers, SNAI1 destabilisation and impaired migratory capacity of cancer cells. Reversely, STAMBPL1 expression reprogrammes cells towards a mesenchymal phenotype. A significant STAMBPL1-SNAI1 co-signature was observed across multiple tumour types. Importantly, STAMBPL1 is highly expressed in metastatic tissues compared to matched primary tumour of the same lung cancer patient and its expression predicts poor prognosis. CONCLUSIONS: Our study provides a novel concept of oncogenic regulation of a DUB and presents a new role and predictive value of STAMBPL1 in the EMT process across multiple carcinomas.

miR-126-5p targets Malate Dehydrogenase 1 in non-small cell lung carcinomas.

Malate Dehydrogenase (MDH) 1 has recently been shown to be highly expressed and display prognostic value in non-small cell lung carcinomas (NSCLCs). However, it is not known how MDH1 expression is regulated and there is no current molecular or chemical strategy that specifically targets MDH1. This may be due to structural and enzymatic similarities with its isoenzyme, malate dehydrogenase 2 (MDH2). However, MDH1 and MDH2 are encoded by distinct genes and this opens up the possibility for modulation at the expression level. Here, we screened in silico for microRNAs (miRs) that selectively targets the 3'UTR region of MDH1. These analyses revealed that mir-126-5p has three binding sites in the 3'UTR region of MDH1. Additionally, we show that expression of miR-126-5p suppresses the enzymatic activity of MDH1, mitochondrial respiration and caused cell death in NSCLC cell lines.

Sodium arsenite down-regulates the expression of X-linked inhibitor of apoptosis protein via translational and post-translational mechanisms in hepatocellular carcinoma.

X-linked inhibitor of apoptosis protein (XIAP) is a member of the inhibitors of apoptosis protein (IAP) family, and has been reported to exhibit elevated expression levels in hepatocellular carcinoma (HCC) and promote cell survival, metastasis and tumor recurrence. Targeting XIAP has proven effective for the inhibition of cancer cell proliferation and restoration of cancer cell chemosensitivity. Arsenic (or sodium arsenite) is a potent anti-tumor agent used to treat patients with acute promyelocytic leukemia (APL). Additionally, arsenic induces cell growth inhibition, cell cycle arrest and apoptosis in human HCC cells. In this study, we identified XIAP as a target for sodium arsenite-induced cytotoxicity in HCC. The exposure of HCC cell lines to sodium arsenite resulted in inhibition of XIAP expression in both a dose- and time-dependent manner. Sodium arsenite blocked the de novo XIAP synthesis and the activity of its internal ribosome entry site (IRES) element. Moreover, treatment with sodium arsenite decreased the protein stability of XIAP and induced its ubiquitin-proteasomal degradation. Overexpression of XIAP attenuated the pro-apoptotic effect of sodium arsenite in HCC. Taken together, our data demonstrate that sodium arsenite suppresses XIAP expression via translational and post-translational mechanisms in HCC.

Structural and functional conservation of CLEC-2 with the species-specific regulation of transcript expression in evolution.

CLEC-2 was first identified by sequence similarity to C-type lectin-like molecules with immune functions and has been reported as a receptor for the platelet-aggregating snake venom toxin rhodocytin and the endogenous sialoglycoprotein podoplanin. Recent researches indicate that CLEC-2-deficient mice were lethal at the embryonic stage associated with disorganized and blood-filled lymphatic vessels and severe edema. In view of a necessary role of CLEC-2 in the individual development, it is of interest to investigate its phylogenetic homology and highly conserved functional regions. In this work, we reported that CLEC-2 from different species holds with an extraordinary conservation by sequence alignment and phylogenetic tree analysis. The functional structures including N-linked oligosaccharide sites and ligand-binding domain implement a structural and functional conservation in a variety of species. The glycosylation sites (N120 and N134) are necessary for the surface expression CLEC-2. CLEC-2 from different species possesses the binding activity of mouse podoplanin. Nevertheless, the expression of CLEC-2 is regulated with a species-specific manner. The alternative splicing of pre-mRNA, a regulatory mechanism of gene expression, and the binding sites on promoter for several key transcription factors vary between different species. Therefore, CLEC-2 shares high sequence homology and functional identity. However the transcript expression might be tightly regulated by different mechanisms in evolution.

Interstitial lung disease independently associated with higher risk for COVID-19 severity and mortality: A meta-analysis of adjusted effect estimates.

OBJECTIVE: The aim of this study was to address the association between interstitial lung disease and the risk for severity and mortality among patients with coronavirus disease 2019 (COVID-19). METHODS: The electronic databases of PubMed, Web of Science and EMBASE were systematically searched. The pooled effect size with 95 % confidence interval (CI) was computed by a random-effects meta-analysis model. Heterogeneity test, sensitivity analysis, subgroup analysis, meta-regression analysis, Begg's test and Egger's test were performed. RESULTS: A total of sixteen eligible studies with 217,260 COVID-19 patients were enrolled in this meta-analysis. The findings based on adjusted effect estimates indicated that pre-existing interstitial lung disease was significantly associated with higher risk for COVID-19 severity (pooled effect = 1.34 [95 % CI: 1.16-1.55]) and mortality (pooled effect = 1.26 [95 % CI: 1.09-1.46]). Consistent results were observed in the subgroup analysis stratified by sample size, age, the percentage of male patients, study design, setting, the methods for adjustment and the factors for adjustment. The results of meta-regression demonstrated that sample size, age and region might be the potential sources of heterogeneity. Sensitivity analysis exhibited that our results were stable and robust. No publication bias was observed in Egger's test and Begg's test. CONCLUSION: This meta-analysis on the basis of adjusted effect estimates demonstrated that pre-existing interstitial lung disease was independently associated with significantly higher risk for COVID-19 severity and mortality.

Painless aortic dissection presenting as pseudo ileus: A case report.

Aortic dissection is a serious acute cardiovascular disease with rapid onset, progression and a high mortality rate. Due to the range of different branching vessels involved, the clinical symptoms are complex and diverse. The typical clinical symptom is a severe tearing pain in the chest, back or abdomen, but some patients also have atypical symptoms, which are easily missed or misdiagnosed and can be life-threatening. The present study reports a case of painless type B aortic dissection, initially diagnosed as ileus. The objective of this study is to enhance the clinical understanding of painless aortic dissection so that the disease can be quickly and accurately detected, and treated in a timely manner, thereby improving patient outcomes.

CDK11p46 and RPS8 associate with each other and suppress translation in a synergistic manner.

CDK11p46, a 46kDa isoform of the PITSLRE kinase family, is a key mediator of cell apoptosis, while the precise mechanism remains to be elucidated. By using His pull-down and mass spectrometry analysis, we identified the ribosomal protein S8 (RPS8), a member of the small subunit ribosome, as an interacting partner of CDK11p46. Further analysis confirmed the association of CDK11p46 and RPS8 in vitro and in vivo, and revealed that RPS8 was not a substrate of CDK11p46. Moreover, RPS8 and CDK11p46 synergize to inhibit the translation process both in cap- and internal ribosomal entry site (IRES)-dependent way, and sensitize cells to Fas ligand-induced apoptosis. Taken together, our results provide evidence for the novel role of CDK11p46 in the regulation of translation and cell apoptosis.

Polymerase chain reaction detection of Lactobacillus acidophilus in human oral cavity and fecal samples after 2-week consumption of yoghurt.

OBJECTIVE: To investigate whether short-term daily consumption of yoghurt leads to colonization by Lactobacillus acidophilus in a group of human subjects who were initially totally devoid of L. acidophilus in their oral cavities. MATERIAL AND METHODS: Twenty-three volunteers consumed yogurt containing L. acidophilus during a 14-day trial stage. Oral and fecal samples were collected at the clearance stage and at the post-yoghurt intake stage until L. acidophilus was found. Standard polymerase chain reaction methods using specific primers were adopted for the detection and identification of L. acidophilus. RESULTS: The isolation frequency decreased rapidly 72 h after stopping intake of yoghurt. After 1 week, L. acidophilus was absent in all oral samples. Non-significant differences were found between the survival rates of L. acidophilus in samples of saliva, plaque, tongue surface, and buccal mucosa. L. acidophilus was also found to remain in the gastrointestinal tract for longer than in the oral cavity. CONCLUSION: Allochthonous L. acidophilus is not likely to permanently colonize the oral cavity and intestine.

Quantitative proteomic analysis of temporal lysosomal proteome and the impact of the KFERQ-like motif and LAMP2A in lysosomal targeting.

Autophagic pathways are regulated mechanisms that play important roles in lysosome-mediated cellular degradation. Yet, the contribution of different autophagic pathways in lysosomal targeting, and characterization of the extent and specificity in their degradome remains largely uncharacterized. By undertaking a multiplex quantitative mass spectrometry approach, we have previously analyzed the lysosomal proteome during chaperone-mediated autophagy (CMA)-stimulated conditions in cancer cells. Here, we have extended our multiplex quantitative mass spectrometry and bioinformatics analysis on the proteome from isolated lysosomes to gain a comprehensive view of the temporal enriched lysosomal content upon non-macroautophagy-activated conditions. In parallel, we describe the functional dependency of LAMP2A on, and to what degree the presence of KFERQ-like motifs in proteins influences, their lysosomal targeting. These findings establish a framework for a better understanding of the degradome mediated by autophagic pathways beyond macroautophagy, and present characterization of the impact of LAMP2A in lysosomal targeting in cancer cells.Abbreviations: CMA: chaperone-mediated autophagy; ER: endoplasmic reticulum; EIF4A1: eukaryotic translation initiation factor 4A1; eMI: endosomal microautophagy; FC: fold change; GO: gene ontology; ISR: integrated stress response; LAMP2A: lysosomal associated membrane protein 2A; MA: macroautophagy; MI: microautophagy; MS: mass spectrometry; PCA: principal component analysis; TAX1BP1: Tax1 binding protein 1.

An electron microscopy study of the diversity of Streptococcus sanguinis cells induced by lysozyme in vitro.

Bacterial virulence could be altered by the antimicrobial agents of the host. Our aim was to identify the damage and survival of Streptococcus sanguinis induced by lysozymes in vitro and to analyse the potential of oral microorganisms to shirk host defences, which cause infective endocarditis. S. sanguinis ATCC 10556 received lysozyme at concentrations of 12.5, 25, 50 and 100 microg/ml. Cells were examined by electron microscopy. The survival was assessed by colony counting and construction of a growth curve. Challenged by lysozymes, cells mainly exhibited cell wall damage, which seemed to increase with increasing lysozyme concentration and longer incubation period in the presence of ions. Cells with little as well as apparent lesion were observed under the same treatment set, and anomalous stick and huge rotund bodies were occasionally observed. After the removal of the lysozyme, some damaged cells could be reverted to its original form with brain heart infusion (BHI), and their growth curve was similar to the control cells. After further incubation in BHI containing lysozyme, S. sanguinis cell damage stopped progressing, and their growth curve was also similar to the control cells. The results suggested that the S. sanguinis lesions caused by the lysozyme in the oral cavity may be nonhomogeneous and that some damaged cells could self-repair and survive. It also indicated that S. sanguinis with damaged cell walls may survive and be transmitted in the bloodstream.

Effect of toothpaste containing d-limonene on natural extrinsic smoking stain: a 4-week clinical trial.

PURPOSE: To determine whether natural smoking stain could be removed/inhibited effectively by a toothpaste containing 5% d-limonene. For comparison and contrast, the effects of d-limonene on tea stain were also assessed. METHODS: The design was a randomized controlled double-blind trial with parallel groups. Toothpastes were: A: positive control with perlite whitening formulation; B: A+5% d-limonene; C: D + 5% d-limonene; D: negative control. The extrinsic stains were measured using Lobene Stain Index. Following baseline examination, all subjects were randomly assigned to one of the four toothpaste groups and instructed to brush with the assigned products twice daily. Subjects returned to the clinic after 4-week brushing for stain removal assessment, then all extrinsic stains, plaque and supragingival calculus were removed and use of assigned products was continued for another 4 weeks, and the stain scores were repeated for inhibition assessment. RESULTS: A total of 408 subjects, 201 with smoking stains and 207 with tea stains, participated in the trial. 5% d-limonene combined with Perlite whitening formulation significantly reduced stain scores both for smoking stain removal and inhibition (P < 0.05). Furthermore, 5% d-limonene alone (in negative formulation) exhibited an additional advantage for smoking stain inhibition (P < 0.05), but the advantage was not found for long-standing smoking stain removal (P > 0.05). The additional advantage of 5% d-limonene was shown neither for removal nor for inhibition in the tea stain study (P > 0.05). All test products were well tolerated over the study period.

Competition between yogurt probiotics and periodontal pathogens in vitro.

OBJECTIVE: To investigate the competition between probiotics in bio-yogurt and periodontal pathogens in vitro. MATERIAL AND METHODS: The antimicrobial activity of bio-yogurt was studied by agar diffusion assays, using eight species of putative periodontal pathogens and a 'protective bacteria' as indicator strains. Four probiotic bacterial species (Lactobacillus bulgaricus, Streptococcus thermophilus, Lactobacillus acidophilus, and Bifidobacterium) were isolated from yogurt and used to rate the competitive exclusion between probiotics and periodontal pathogens. RESULTS: Fresh yogurt inhibited all the periodontal pathogens included in this work, showing inhibition zones ranging from 9.3 (standard deviation 0.6) mm to 17.3 (standard deviation 1.7) mm, whereas heat-treated yogurt showed lower antimicrobial activity. In addition, neither fresh yogurt nor heat-treated yogurt inhibited the 'protective bacteria', Streptococcus sanguinis. The competition between yogurt probiotics and periodontal pathogens depended on the sequence of inoculation. When probiotics were inoculated first, Bifidobacterium inhibited Porphyromonas gingivalis, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans, Porphyromonas circumdentaria, and Prevotella nigrescens; L. acidophilus inhibited P. gingivalis, A. actinomycetemcomitans, P. circumdentaria, P. nigrescens, and Peptostreptococcus anaerobius; L. bulgaricus inhibited P. gingivalis, A. actinomycetemcomitans, and P. nigrescens; and S. thermophilus inhibited P. gingivalis, F. nucleatum, and P. nigrescens. However, their antimicrobial properties were reduced when both species (probiotics and periodontal pathogens) were inoculated simultaneously. When periodontal pathogens were inoculated first, Prevotella intermedia inhibited Bifidobacterium and S. thermophilus. CONCLUSIONS: The results demonstrated that bio-yogurt and the probiotics that it contains are capable of inhibiting specific periodontal pathogens but have no effect on the periodontal protective bacteria.

Model-based optimized phase-deviation deep brain stimulation for Parkinson 's disease.

High-frequency deep brain stimulation (HF-DBS) of the subthalamic nucleus (STN), globus pallidus interna (GPi) and globus pallidus externa (GPe) are often considered as effective methods for the treatment of Parkinson's disease (PD). However, the stimulation of a single nucleus by HF-DBS can cause specific physical damage, produce side effects and usually consume more electrical energy. Therefore, we use a biophysically-based model of basal ganglia-thalamic circuits to explore more effective stimulation patterns to reduce adverse effects and save energy. In this paper, we computationally investigate the combined DBS of two nuclei with the phase deviation between two stimulation waveforms (CDBS). Three different stimulation combination strategies are proposed, i.e., STN and GPe CDBS (SED), STN and GPi CDBS (SID), as well as GPi and GPe CDBS (GGD). Resultantly, it is found that anti-phase CDBS is more effective in improving parkinsonian dynamical properties, including desynchronization of neurons and the recovery of the thalamus relay ability. Detailed simulation investigation shows that anti-phase SED and GGD are superior to SID. Besides, the energy consumption can be largely reduced by SED and GGD (72.5% and 65.5%), compared to HF-DBS. These results provide new insights into the optimal stimulation parameter and target choice of PD, which may be helpful for the clinical practice.

Targetome analysis of chaperone-mediated autophagy in cancer cells.

Chaperone-mediated autophagy (CMA) is a lysosomal degradation pathway of select soluble proteins. Nearly one-third of the soluble proteins are predicted to be recognized by this pathway, yet only a minor fraction of this proteome has been identified as CMA substrates in cancer cells. Here, we undertook a quantitative multiplex mass spectrometry approach to study the proteome of isolated lysosomes in cancer cells during CMA-activated conditions. By integrating bioinformatics analyses, we identified and categorized proteins of multiple cellular pathways that were specifically targeted by CMA. Beyond verifying metabolic pathways, we show that multiple components involved in select biological processes, including cellular translation, was specifically targeted for degradation by CMA. In particular, several proteins of the translation initiation complex were identified as bona fide CMA substrates in multiple cancer cell lines of distinct origin and we show that CMA suppresses cellular translation. We further show that the identified CMA substrates display high expression in multiple primary cancers compared to their normal counterparts. Combined, these findings uncover cellular processes affected by CMA and reveal a new role for CMA in the control of translation in cancer cells. Abbreviations: 6-AN: 6-aminonicotinamide; ACTB: actin beta; AR7: atypical retinoid 7; CHX: cycloheximide; CMA: chaperone-mediated autophagy; CQ: chloroquine; CTS: cathepsins; DDX3X: DEAD-box helicase 3 X-linked; EEF2: eukaryotic translation elongation factor 2; EIF4A1: eukaryotic translation initiation factor 4A1; EIF4H: eukaryotic translation initiation factor 4H; GEO: Gene Expression Omnibus; GO: Gene Ontology; GSEA: gene set enrichment analysis; HK2: hexokinase 2; HSPA8/HSC70: heat shock protein family A (Hsp70) member 8; LAMP: lysosomal-associated membrane protein; LDHA: lactate dehydrogenase A; NES: normalized enrichment score; NFKBIA: NFKB inhibitor alpha; PCA: principle component analysis; PQ: paraquat; S.D.: standard deviation; SUnSET: surface sensing of translation; TMT: tandem mass tags; TOMM40/TOM40: translocase of outer mitochondrial membrane 40.

Chromosome alignment maintenance requires the MAP RECQL4, mutated in the Rothmund-Thomson syndrome.

RecQ-like helicase 4 (RECQL4) is mutated in patients suffering from the Rothmund-Thomson syndrome, a genetic disease characterized by premature aging, skeletal malformations, and high cancer susceptibility. Known roles of RECQL4 in DNA replication and repair provide a possible explanation of chromosome instability observed in patient cells. Here, we demonstrate that RECQL4 is a microtubule-associated protein (MAP) localizing to the mitotic spindle. RECQL4 depletion in M-phase-arrested frog egg extracts does not affect spindle assembly per se, but interferes with maintaining chromosome alignment at the metaphase plate. Low doses of nocodazole depolymerize RECQL4-depleted spindles more easily, suggesting abnormal microtubule-kinetochore interaction. Surprisingly, inter-kinetochore distance of sister chromatids is larger in depleted extracts and patient fibroblasts. Consistent with a role to maintain stable chromosome alignment, RECQL4 down-regulation in HeLa cells causes chromosome misalignment and delays mitotic progression. Importantly, these chromosome alignment defects are independent from RECQL4's reported roles in DNA replication and damage repair. Our data elucidate a novel function of RECQL4 in mitosis, and defects in mitotic chromosome alignment might be a contributing factor for the Rothmund-Thomson syndrome.

Effect of compounds of Galla chinensis and their combined effects with fluoride on remineralization of initial enamel lesion in vitro.

OBJECTIVE: To investigate the effect of chemical compounds of Galla chinensis and their combined effects with fluoride on remineralization of artificial early enamel caries. METHOD: Bovine enamel blocks with in vitro produced initial lesion were used. The lesions were subjected to a pH-cycling regime for 12 days. Each daily cycle included 4x 1min applications with one of six treatments group A: 1000ppm F aq. (as NaF, positive control); group B: deionized water (DDW, negative control); group C: 4000ppm crude aqueous extract of G. chinensis (GCE); group D: 4000ppm gallic acid; group E: 4000ppm GCE with 1000ppm F; group F: 4000ppm gallic acid with 1000ppm F. The enamel specimens were analyzed by transverse microradiography. Integrated mineral loss (IML) and lesion depth (LD) were measured and mineral content in the surface layer and lesion body were calculated. RESULTS: The LD and IML were significantly different among the different treatment groups. GCE and gallic acid could reduce LD and IML significantly compared with DDW. Groups E and F showed the shallowest lesion. In the groups with gallic acid (groups D and F), mineral deposition predominated in the surface layer. In groups with GCE (groups C and E), more mineral deposition occurred in the lesion body. CONCLUSION: The chemical compounds of G. chinensis were able to enhance remineralization of dental enamel. They also had combined effects with fluoride on enhancing remineralization.