Sandblasting increases the microtensile bond strength between resin and sclerotic dentin in noncarious cervical lesions.

PURPOSE: To evaluate the effect of sandblasting on the microtensile strength between sclerotic dentin and resin composite. METHODS: 32 premolars with noncarious cervical lesions (NCCLs) were collected, and the teeth were randomly assigned to the control group (C group) and the sandblasted group (S group). Teeth in the S group were sandblasted with 110 µm Al2O3 particles at a pressure of 75 psi, while those in the C group received no further treatment. The characteristics of the tooth surface were observed by scanning electron microscopy (SEM), and the relative area of open dentin tubules (OTs) was calculated by IPP6.0 software. Surface roughness (Ra) was also assessed. The noncarious cervical lesions of all teeth were restored with a resin composite and subsequently sectioned into sticks to measure the microtensile bond strength (µTBS). RESULTS: The mean ± SD µTBS (in MPa) of the sandblasted group was 17.9 ± 0.69 and 14.23 ± 0.44 in the control group (P< 0.05). The relative area of OTs at the gingival wall of the sandblasted group was 69.74 ± 5.23%, and 47.24 ± 7.67% in the control group (P< 0.05). The average surface roughness (µm) was 1.01 ± 0.05 in the sandblasted group and 0.16 ± 0.03 in the control group. Sandblasting could increase the bond strength of sclerotic dentin and resin restorations. CLINICAL SIGNIFICANCE: After sandblasting, the microtensile strength of sclerotic dentin on the surface of noncarious cervical lesions increased, prolonging the resin adhesion longevity. Sandblasting could also alleviate the pain of patients during the treatment process and achieve a minimally invasive treatment.

Symptom burden survey and symptom clusters in patients with cervical cancer: a cross-sectional survey.

PURPOSE: The purpose of this study is to determine the incidence and severity of symptoms of patients with cervical cancer within 6 months after radiotherapy and chemotherapy, form a symptom burden report, evaluate the distribution characteristics of symptoms, identify symptom clusters, and provide a basis for clinical doctors and nurses to improve the symptom management of patients with cervical cancer after radiotherapy and chemotherapy. METHODS: The patients with cervical cancer within 6 months after radiotherapy and chemotherapy were recruited to investigate their symptom burden. Exploratory factor analysis was used to identify symptom clusters. RESULTS: A total of 250 patients participated in the study. The study found that the most common symptom among the 40 symptoms was fatigue, and the most serious symptom was nocturia. Based on the occurrence rate and severity of symptoms, nine symptom clusters were identified, including psycho-emotion-related symptom cluster, pain-disturbed sleep-related symptom cluster, menopausal symptom cluster, tinnitus-dizziness-related symptom cluster, urinary-related symptom cluster, dry mouth-bitter taste-related symptom cluster, intestinal-related symptom cluster, memory loss-numbness-related symptom cluster, and emaciation-related symptom cluster. The three most serious symptom clusters are pain-disturbed sleep-related symptom cluster, urinary-related symptom cluster, and memory loss-numbness-related symptom cluster. CONCLUSION: The symptoms of patients with cervical cancer within 6 months after radiotherapy and chemotherapy are complex, and nine symptom clusters can be identified according to the incidence and severity of symptoms. We can find the potential biological mechanism of each symptom cluster through the discussion of previous mechanism research and clinical research. The number of symptom clusters and the number of symptoms within the symptom cluster are closely related to the symptom evaluation scale selected for the study. Therefore, the symptom cluster study urgently needs a targeted symptom evaluation scale that can comprehensively reflect the patient's condition.

Porphyromonas gingivalis Activation of Tumor-Associated Macrophages via DOK3 Promotes Recurrence of Oral Squamous Cell Carcinoma.

BACKGROUND Oral squamous cell carcinoma (OSCC) is the most common head and neck malignancy, characterized by high recurrence rate resulting in poor prognosis. Porphyromonas gingivalis, most closely correlated with chronic periodontitis, is increasingly thought to play a significant role in OSCC development via influencing tumor-associated macrophages. However, its specific function remains unclear. In this study, we attempted to explore the mechanism of action of P. gingivalis in the recurrence of OSCC by bioinformatics analysis, to lay a foundation for subsequent basic experiments. MATERIAL AND METHODS The P. gingivalis-infected macrophage microarray dataset (GSE24897) and the OSCC advanced relapse patient microarray dataset (GSE87593) were retrieved from the Gene Expression Omnibus (GEO) database. Differentially-expressed genes (DEGs) were screened using R system, and the intersected DEGs were analyzed for functional enrichment, and protein-protein interaction (PPI) networks were constructed. The expression of significant DEG in GSE24897 microarray was assessed to determine its effect on macrophage immune infiltration in pan-cancer by applying the TIMER 2.0 repository. To detect the expression of DOK3 in OSCC specimens, immunohistochemical (ICH) assay was used. RESULTS A total of 106 co-expressed DEGs were upregulated and 131 were downregulation. The biological processes were mainly enriched in DNA-templated transcription terms, the cellular component enrichment was mainly enriched in the nucleus terms, and the molecular function enrichment was mainly enriched in protein-binding function terms. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis found that the DEGs were mainly enriched in the MAPK signaling pathway. Overall analysis of the PPI network showed a significant aggregation, with the top 10 hub co-expressed genes (CASP3, FYN, HNRNPA2B1, NR3C1, RELA, REL, POLR2F, RAN, RHOA, and STAT5B). DOK3 is significantly upregulated in P. gingivalis-infected macrophages, which is associated with macrophage infiltration and differentiation. There was more positive DOK3 staining in the group with P. gingivalis infection. CONCLUSIONS P. gingivalis can affect the recurrence of OSCC by increasing the expression of DOK3 in TAMs, which may be involved in activation of signaling pathways such as TNF and MAPK.

Characterization of the ABC Transporter G Subfamily in Pomegranate and Function Analysis of PgrABCG14.

ATP-binding cassette subfamily G (ABCG) proteins play important roles in plant growth and development by transporting metabolites across cell membranes. To date, the genetic characteristics and potential functions of pomegranate ABCG proteins (PgrABCGs) have remained largely unknown. In this study, we found that 47 PgrABCGs were divided into five groups according to a phylogenetic analysis; groups I, II, III, and IV members are half-size proteins, and group V members are full-size proteins. PgrABCG14, PgrABCG21, and PgrABCG47 were highly expressed in the inner seed coat but had very low expression levels in the outer seed coat, and the expression levels of these three PgrABCG genes in the inner seed coats of hard-seeded pomegranate 'Dabenzi' were higher than those of soft-seeded pomegranate 'Tunisia'. In addition, the expression of these three PgrABCG genes was highly correlated with the expression of genes involved in lignin biosynthesis and hormone signaling pathways. The evolution of PgrABCG14 presents a highly similar trend to the origin and evolution of lignin biosynthesis during land plant evolution. Ectopic expression of PgrABCG14 in Arabidopsis promoted plant growth and lignin accumulation compared to wild type plants; meanwhile, the expression levels of lignin biosynthesis-related genes (CAD5, C4H, and Prx71) and cytokinin response marker genes (ARR5 and ARR15) were significantly upregulated in transgenic plants, which suggests the potential role of PgrABCG14 in promoting plant growth and lignin accumulation. Taken together, these findings not only provide insight into the characteristics and evolution of PgrABCGs, but also shed a light on the potential functions of PgrABCGs in seed hardness development.

Preparation of Electrospun Active Molecular Membrane and Atmospheric Free Radicals Capture.

We load the natural active molecules onto the spin film in an array using electrospinning techniques. The electrospun active molecular membranes we obtain in optimal parameters exhibit excellent capacity for scavenging radical. The reaction capacity of three different membranes for free radicals are shown as follow, glycyrrhizin acid membrane > quercetin membrane > α-mangostin membrane. The prepared active molecular electrospun membranes with a large specific surface area and high porosity could increase the interaction area between active molecules and free radicals. Additionally, it also has improved anti-airflow impact strength, anti-contaminant air molecular interference ability, and the ability to capture free radicals.

Wnt5a promotes inflammatory responses via nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways in human dental pulp cells.

Wnt5a has been found recently to be involved in inflammation regulation through a mechanism that remains unclear. Immunohistochemical staining of infected human dental pulp and tissue from experimental dental pulpitis in rats showed that Wnt5a levels were increased. In vitro, Wnt5a was increased 8-fold in human dental pulp cells (HDPCs) after TNF-α stimulation compared with control cells. We then investigated the role of Wnt5a in HDPCs. In the presence of TNF-α, Wnt5a further increased the production of cytokines/chemokines, whereas Wnt5a knockdown markedly reduced cytokine/ chemokine production induced by TNF-α. In addition, in HDPCs, Wnt5a efficiently induced cytokine/chemokine expression and, in particular, expression of IL-8 (14.5-fold) and CCL2 (25.5-fold), as assessed by a Luminex assay. The cytokine subsets regulated by Wnt5a overlap partially with those induced by TNF-α. However, no TNF-α and IL-1ß was detected after Wnt5a treatment. We then found that Wnt5a alone and the supernatants of Wnt5a-treated HDPCs significantly increased macrophage migration, which supports a role for Wnt5a in macrophage recruitment and as an inflammatory mediator in human dental pulp inflammation. Finally, Wnt5a participates in dental pulp inflammation in a MAPK-dependent (p38-, JNK-, and ERK-dependent) and NF-κB-dependent manner. Our data suggest that Wnt5a, as an inflammatory mediator that drives the integration of cytokines and chemokines, acts downstream of TNF-α.

Metabolic interaction between anthocyanin and lignin biosynthesis is associated with peroxidase FaPRX27 in strawberry fruit.

Plant phenolics have drawn increasing attention due to their potential nutritional benefits. Although the basic reactions of the phenolics biosynthetic pathways in plants have been intensively analyzed, the regulation of their accumulation and flux through the pathway is not that well established. The aim of this study was to use a strawberry (Fragaria × ananassa) microarray to investigate gene expression patterns associated with the accumulation of phenylpropanoids, flavonoids, and anthocyanins in strawberry fruit. An examination of the transcriptome, coupled with metabolite profiling data from different commercial varieties, was undertaken to identify genes whose expression correlated with altered phenolics composition. Seventeen comparative microarray analyses revealed 15 genes that were differentially (more than 200-fold) expressed in phenolics-rich versus phenolics-poor varieties. The results were validated by heterologous expression of the peroxidase FaPRX27 gene, which showed the highest altered expression level (more than 900-fold). The encoded protein was functionally characterized and is assumed to be involved in lignin formation during strawberry fruit ripening. Quantitative trait locus analysis indicated that the genomic region of FaPRX27 is associated with the fruit color trait. Down-regulation of the CHALCONE SYNTHASE gene and concomitant induction of FaPRX27 expression diverted the flux from anthocyanins to lignin. The results highlight the competition of the different phenolics pathways for their common precursors. The list of the 15 candidates provides new genes that are likely to impact polyphenol accumulation in strawberry fruit and could be used to develop molecular markers to select phenolics-rich germplasm.

Cellulose fiber-based and engineered capillary foam toward a sustainable, recyclable, and high-performance cushioning structural material.

Foam materials have been widely used in cushioning packaging to ensure the integrity of products inside by absorbing energy and preventing collision. However, the extensive use of petroleum-based plastic foams may exacerbate environmental pollution and consume large amounts of energy. Therefore, there has been an increasing focus on producing high-performance and environmentally friendly foams in recent years. In this study, we developed a simple approach for manufacturing cellulose fiber-based capillary foams featuring superior stability and three-dimensional (3D) backbone network cross-linking structure composed of polyvinyl alcohol (PVA) and cationic starch (CS). The resultant capillary foam showed low density (0.154 g/cm3), superior mechanical properties (elastic modulus ranging from 77 to 501 kPa), high energy absorbing efficiency (32.8 %), and low cushioning coefficient (3.0). Besides, the end-of-life cellulose fiber-based capillary foam can be easily recycled for use, showing an attractive closed-loop cycle process. This study presents a unique option for creating affordable, eco-friendly, and malleable foams, demonstrating the potential to substitute the currently used petroleum-based foams in the packaging, food, and transport industries.

Recent advances in understanding the biochemical and molecular mechanism of diabetic cardiomyopathy.

Cardiovascular complications account for significant morbidity and mortality in the diabetic population. Diabetic cardiomyopathy (DCM), a prominent cardiovascular complication, has been recognized as a microvascular disease that may lead to heart failure. During the past few decades, research progress has been made in investigating the pathophysiology of the disease; however, the exact molecular mechanism has not been elucidated, making therapeutic a difficult task. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C, free fatty acid and oxidative stress and other related factors that are implicated in the pathophysiology of the DCM. An understanding of the biochemical and molecular changes especially early in the DCM may lead to new and effective therapies toward prevention and amelioration of DCM, which is important for the millions of individuals who already have or are likely to develop the disease before a cure becomes available.

Supramolecular aggregation/disaggregation-based molecular sensing: a review focused on investigations from China.

Supramolecular aggregation and disaggregation induced by external stimuli can impact the optical or electrical signals of the aggregates/constituting units (receptors). Therefore, manipulating supramolecular aggregation/disaggregation has recently been employed to construct novel and promising photoluminescence (PL)-based sensing and recognition systems. The sensing systems were capable of substantially enhancing the sensitivity, relying on cooperative interactions occurring in the assembly/disassembly processes (mostly operating in emission turned-on or emission-enhanced mode). This review focuses mainly on recent advances in the new emerging PL-based sensing platforms, based on manipulating the behaviours of supramolecular aggregation/disaggregation, including aggregation-induced emission (AIE), metallophilic interactions-related sensing (metallophilic interactions-induced aggregation/disaggregation), metal coordination polymers-related sensing, and other sensing systems involving supramolecular aggregation/disaggregation. In particular, those sensing systems developed by scientists in China are summarized and highlighted.

Correlations of podocyte injury with glucose regulated protein 78 expression and proteinuria in patients with diabetic nephropathy.

OBJECTIVE: To explore the podocyte injury in patients with diabetic nephropathy (DN) and analyze its relationship with glucose regulated protein 78 (GRP78) and proteinuria. METHODS: The clinical data of 48 patients diagnosed as DN by renal biopsy were reviewed. All patients were divided into two groups according to proteinuria (>3.5 g/d, n=31 and 3.5 g/d, n=17). The density of podocytes was illustrated by immunohistochemistry staining of Wilms tumor-1 (WT-1), and the immunofluorescence double-staining results of synaptopodin and GRP78 in podocytes were detected. RESULTS: The podocyte dentistry of urine protein > 3.5 g/d group was significantly lower than that of urine protein>3.5 g/d group urine protein<3.5 g/d group(P=0.003), and it was negatively correlated with proteinuria (P=0.005). The expressions of synaptopodin and GRP78 in podocytes were also negatively correlated with proteinuria (P=0.004 and P=0.001). CONCLUSION: The podocyte injury is aggravated with increased proteinuria in DN patients, along with the decrease of the adaptive ability of endoplasmic reticulum to stress.

Endogenous hydrogen sulfide counteracts polystyrene nanoplastics-induced mitochondrial apoptosis and excessive autophagy via regulating Nrf2 and PGC-1α signaling pathway in mouse spermatocyte-derived GC-2spd(ts) cells.

Nanoplastics (NaPs) has reported to accumulate in the testes and cause degeneration in the seminiferous tubules. Additionally, exogenous hydrogen sulfide (H2S) is proposed to enhance tolerance to oxidative stress. The current work aimed to investigate the mechanisms of NaPs-induced reproductive toxicity in vitro and probable reproductive protection by endogenous H2S. We firstly found that 80 nm fluorescent NaPs could enter into GC-2spd(ts) cells by fluorescent inverted microscope. In addition, we demonstrated that NaPs-induced could induce ROS-dependent mitochondrial apoptosis and autophagy in vitro. Our results showed that the H2S donor NaHS ameliorated NaPs-triggered mitochondrial apoptosis and autophagy in GC-2spd(ts) cells. Moreover, NaPs treatment did not change the interaction between nuclear factor erythroid-derived 2-related factor (Nrf2) and Kelch-like ECH associated protein 1 (Keap1), while inhibiting nuclear accumulation of Nrf2 protein was observed. Meanwhile, NaHS weakened this interaction, subsequently improving antioxidant ability via increasing the protein levels of heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase quinone 1 (NQO1). Further, invitro experiments showed that NaPs-induced reproductive toxicity associated with reducing PGC-1α. Meanwhile, NaPs-induced higher expression PGC-1α was further enhanced by NaHS co-treatment. Together, this study highlight that exogenous H2S should be an essential therapeutic approach to alleviate NaPs-induced reproductive toxicity via regulating Nrf2/PGC-1α signal.

Regulation of host factor γ-H2AX level and location by enterovirus A71 for viral replication.

Numerous viruses manipulate host factors for viral production. We demonstrated that human enterovirus A71 (EVA71), a primary causative agent for hand, foot, and mouth disease (HFMD), increased the level of the DNA damage response (DDR) marker γ-H2AX. DDR is primarily mediated by the ataxia telangiectasia mutated (ATM), ATM and Rad3-related (ATR), or DNA-dependent protein kinase (DNA-PK) pathways. Upregulation of γ-H2AX by EVA71 was dependent on the ATR but not the ATM or DNA-PK pathway. As a nuclear factor, there is no previous evidence of cytoplasmic distribution of γ-H2AX. However, the present findings demonstrated that EVA71 encouraged the localization of γ-H2AX to the cytoplasm. Of note, γ-H2AX formed a complex with structural protein VP3, non-structural protein 3D, and the viral genome. Treatment with an inhibitor or CRISPR/Cas9 technology to decrease or silence the expression of γ-H2AX decreased viral genome replication in host cells; this effect was accompanied by decreased viral protein expression and virions. In animal experiments, caffeine was used to inhibit DDR; the results revealed that caffeine protected neonatal mice from death after infection with EVA71, laying the foundation for new therapeutic applications of caffeine. More importantly, in children with HFMD, γ-H2AX was upregulated in peripheral blood lymphocytes. The consistent in vitro and in vivo data on γ-H2AX from this study suggested that caffeine or other inhibitors of DDR might be novel therapeutic agents for HFMD.

Clinical Outcomes Following Immediate Loading of Single-Tooth Implants in the Esthetic Zone: A Systematic Review and Meta-Analysis.

PURPOSE: To identify whether or not immediate loading yields different clinical outcomes from conventional loading of single-tooth implants in the esthetic zone. MATERIALS AND METHODS: Various databases (MEDLINE/PubMed, Cochrane [CENTRAL], and Embase) were searched electronically to find articles published in the English language from January 2000 to April 2018. Only randomized controlled clinical trials (RCTs) that compared conventional and immediate implant loading with a minimum follow-up period of 1 year or more were considered. Available data were pooled for meta-analysis using the Review Manager software. RESULTS: Seven RCTs were included. There was no significant difference between immediate and conventional loading protocols on implant survival at the 1-year follow-up (risk ratio [RR] = 0.99; 95% confidence interval [CI]: 0.95 to 1.02). The differences regarding marginal bone loss between the two protocols were statistically insignificant (mean difference [MD] = 0.03 mm; 95% CI: -0.09 to 0.15 mm at the 1-year follow-up, and MD = -0.01 mm; 95% CI: -0.16 to 0.15 mm at the 2-year follow-up). Soft tissue changes following different loading protocols revealed no significant differences in the mesial papillae (MD = 0.30 mm; 95% CI: -0.25 to 0.85 mm), the distal papillae (MD = -0.00 mm; 95% CI: -0.42 to 0.42 mm), and the midfacial mucosa (MD = -0.33 mm; 95% CI: -1.17 to 0.50 mm) at the 1-year follow-up. The esthetic outcomes and patient satisfaction were reported in two and three RCTs, respectively. CONCLUSION: A short-term follow-up of single-tooth implants in the esthetic zone showed that the loading protocols (conventional or immediate loading) are not likely to influence the clinical outcomes, including implant survival and peri-implant stability of soft and hard tissues.

Orthodontic treatment induces Th17/Treg cells to regulate tooth movement in rats with periodontitis.

OBJECTIVES: Here we investigated the regulation of Th17 and Treg cells in orthodontic tooth movement during periodontal inflammation. MATERIALS AND METHODS: Fifty-six SD rats were divided into a control (24 rats) and a tooth movement group during the recovery stage of periodontitis (RM group, 32 rats). Periodontitis was established by silk ligation and local injection of LPS. Orthodontic tooth movement was achieved by nickel-titanium springs on the maxillary first molars. The proportions of Th17 cells and Treg cells were evaluated by flow cytometry. Gene expression of ROR-γt and Foxp3 was determined by real-time PCR. Expression of ROR-γt, Foxp3, RANK, RANKL, and OPG was detected by immunohistochemical staining. Osteoclasts were detected by TRAP staining. Relationships between Th17/Treg cells, osteoclasts, and related factors were estimated by correlation and regression analysis. RESULTS: During orthodontic tooth movement in the recovery stage of periodontitis, the proportion of Th17 cells, ROR-γt, RANK, osteoclasts, and the RANKL/OPG ratio increased and then decreased. The proportion of Treg cells and Foxp3 increased, then decreased, and increased again. Levels of RANKL and OPG increased, then decreased, then increased, and finally decreased. The Th17/Treg ratio initially decreased, then increased, and decreased again. Th17 cells were positively correlated with RANK and RANKL, the RANKL/OPG ratio, and counts of osteoclasts. Treg cells were negatively correlated with RANK expression and numbers of osteoclasts. The Th17/Treg ratio was positively correlated with RANK expression and numbers of osteoclasts. CONCLUSION: Under periodontal inflammation conditions, the Th17/Treg ratio might regulate orthodontic tooth movement through changing osteoclasts metabolism.

Coxsackievirus A6 Induces Necroptosis for Viral Production.

Hand, foot, and mouth disease (HFMD) is a febrile exanthematous disease with typical or atypical symptoms. Typical HFMD is usually caused by enterovirus 71 (EV71) or coxsackievirus A16, while atypical HFMD is usually caused by coxsackievirus A6 (CA6). In recent years, worldwide outbreaks of CA6-associated HFMD have dramatically increased, although the pathogenic mechanism of CA6 is still unclear. EV71 has been established to induce caspase-dependent apoptosis, but in this study, we demonstrate that CA6 infection promotes a distinct pathway of cell death that involves loss of cell membrane integrity. Necrostatin-1, an inhibitor of necroptosis, blocks the cell death induced by CA6 infection, but Z-DEVD-FMK, an inhibitor of caspase-3, has no effect on CA6-induced cell death. Furthermore, CA6 infection up-regulates the expression of the necroptosis signaling molecule RIPK3. Importantly, necrostatin-1 inhibits CA6 viral production, as assessed by its ability to inhibit levels of VP1 protein and genomic RNA and infectious particles. CA6-induced necroptosis is not dependent on the generation of reactive oxygen species; however, viral 3D protein can directly bind RIPK3, which is suggestive of a direct mechanism of necroptosis induction. Therefore, these results indicate that CA6 induces a mechanism of RIPK3-dependent necroptosis for viral production that is distinct from the mechanism of apoptosis induced by typical HFMD viruses.

CMT2Q-causing mutation in the Dhtkd1 gene lead to sensory defects, mitochondrial accumulation and altered metabolism in a knock-in mouse model.

Charcot-Marie-Tooth disease (CMT) is a group of inherited neurological disorders of the peripheral nervous system. CMT is subdivided into two main types: a demyelinating form, known as CMT1, and an axonal form, known as CMT2. Nearly 30 genes have been identified as a cause of CMT2. One of these is the 'dehydrogenase E1 and transketolase domain containing 1' (DHTKD1) gene. We previously demonstrated that a nonsense mutation [c.1455 T > G (p.Y485*)] in exon 8 of DHTKD1 is one of the disease-causing mutations in CMT2Q (MIM 615025). The aim of the current study was to investigate whether human disease-causing mutations in the Dhtkd1 gene cause CMT2Q phenotypes in a mouse model in order to investigate the physiological function and pathogenic mechanisms associated with mutations in the Dhtkd1 gene in vivo. Therefore, we generated a knock-in mouse model with the Dhtkd1Y486* point mutation. We observed that the Dhtkd1 expression level in sciatic nerve of knock-in mice was significantly lower than in wild-type mice. Moreover, a histopathological phenotype was observed, reminiscent of a peripheral neuropathy, including reduced large axon diameter and abnormal myelination in peripheral nerves. The knock-in mice also displayed clear sensory defects, while no abnormalities in the motor performance were observed. In addition, accumulation of mitochondria and an elevated energy metabolic state was observed in the knock-in mice. Taken together, our study indicates that the Dhtkd1Y486* knock-in mice partially recapitulate the clinical phenotypes of CMT2Q patients and we hypothesize that there might be a compensatory effect from the elevated metabolic state in the knock-in mice that enables them to maintain their normal locomotor function.

Conservative pulp treatment for Oehlers type III dens invaginatus: A case report.

BACKGROUND: Diverse presentations of dens invaginatus (DI) and root canal treatment with an immature open apex often pose challenges to dentists. Adequate treatment planning for DI is the main reason for successful approach, i.e., we should consider the shape and depth of the concave folding, the condition of the original pulp, and the growth stage of the root formation. CASE SUMMARY: A 9-year-old girl complained of severe pain of the right maxillary incisor (tooth 12) when chewing for two weeks. Following clinical and radiographic examinations, Oehlers type III DI of tooth 12, with an immature open apical foramen and a symptomatic periapical pathosis, was diagnosed. Cone-beam computed tomography verified the specific spatial and stereoscopic data regarding the communication between the main root canal and pseudo root canal of the involved tooth. After removing the source of infection, a mineral trioxide aggregate was selected to fill and seal the pseudo root canal; additionally, pulp capping of the main canal was performed through the interconnections between the root canals in the middle segment to preserve pulp vitality and enable continual root formation and eventual root apex closure. CONCLUSION: We propose to conduct main root canal pulp capping for DI with communication between the main and pseudo root canals.

Clinical features for 89 deaths of hand, foot and mouth disease in Guangxi, China, 2014.

OBJECTIVES: The aim of this study is to summarize the risk factors of severe Hand, foot and mouth disease (HFMD) and explore the clinical characteristics of pulmonary edema (PE) and non-PE in the deceased patients with HFMD. METHODS: We identified 89 HFMD deaths which were separated into the PE group or non-PE group. Next, patients were divided based on their initial admission to hospitals as stage 1, 2, 3, or 4; at this point, their clinical manifestations were compared. RESULTS: There were 87 cases in the PE group, and 2 cases in the non-PE group. In the PE group, the difference in median time for patients at different stages from onset to symptoms, showed no significant difference (p>0.05). The etiology was detected as a positive rate for enterovirus 71 (EV71) of 89.19%, which showed a more severe course than other etiologies. The white blood cell (WBC) counts, lymphocyte (LYM) counts and creatine kinase MB (CK-MB) counts of patients admitted in different stages increased significantly with severity (p<0.05). CONCLUSIONS: There may be two clinical subtypes, mostly PE and rarely non-PE, in the deceased patients with HMFD. EV71 and risk factors such as an increased WBC count are associated with a severe course of HMFD.