Oral microbial profiles of extrinsic black tooth stain in primary dentition: A literature review.

The extrinsic black tooth stain (EBS) is commonly found in primary dentition. Patients cannot clean the EBS; this can only be done by professional scaling and debridement. It also has a tendency to reform, which significantly compromises children's aesthetics and even affects their quality of life. However, there is no conclusive evidence on the etiology of the EBS. The associations between the EBS and related oral microbial features is one of the research hot topics. No literature review summarized these research progresses in this area. Therefore, we reviewed the literature on the microbiology of the EBS since 1931 and reported as the following 5 aspects: molecular biotechnology, morphological structure and physiochemical characteristics, microbial etiology hypothesis and core microbial characteristics. The EBS is a special dental plaque mainly composed of Gram-positive bacilli and cocci with scattered calcium deposits that acquired salivary pellicle activates. Early studies showed that the Actinomyces was the main pathogenic bacteria. With advances in biological research techniques, the 'core microbiome' was proposed. The potential pathogenic genera were Actinomyces, Prevotella nigrescens, Pseudotropinibacterium, Leptotrichia, Neisseria and Rothia. However, the pathogenic species of the above genera were still unclear. Currently, it is believed that the EBS consists of iron compounds or black substances that oral bacterial metabolism produces or that the bacterial metabolites formed after chemical reactions in the micro-ecological environment.

Implementation of regional Acute Stroke Care Map increases thrombolysis rates for acute ischaemic stroke in Chinese urban area in only 3 months.

BACKGROUND: The rate of intravenous thrombolysis for acute ischaemic stroke remains low in China. We investigated whether the implementation of a citywide Acute Stroke Care Map (ASCaM) is associated with an improvement of acute stroke care quality in a Chinese urban area. METHODS: The ASCaM comprises 10 improvement strategies and has been implemented through a network consisting of 20 tertiary hospitals. We identified 7827 patients with ischaemic stroke admitted from April to October 2017, and 506 patients underwent thrombolysis were finally included for analysis. RESULTS: Compared with 'pre-ASCaM period', we observed an increased rate of administration of tissue plasminogen activator within 4.5 hours (65.4% vs 54.5%; adjusted OR, 1.724; 95% CI 1.21 to 2.45; p=0.003) during 'ASCaM period'. In multivariate analysis models, 'ASCaM period' was associated with a significant reduction in onset-to-door time (114.1±55.7 vs 135.7±58.4 min, p=0.0002) and onset-to-needle time (ONT) (169.2±58.1 vs 195.6±59.3 min, p<0.0001). Yet no change was found in door-to-needle time. Clinical outcomes such as symptomatic intracranial haemorrhage, favourable functional outcome (modified Rankin Scale ≤2) and in-hospital mortality remained unchanged. CONCLUSION: The implementation of ASCaM was significantly associated with increased rates of intravenous thrombolysis and shorter ONT. The ASCaM may, in proof-of-principle, serve as a model to reduce treatment delay and increase thrombolysis rates in Chinese urban areas and possibly other highly populated Asian regions.

Elevation of high-sensitivity cardiac troponin T at admission is associated with increased 3-month mortality in acute ischemic stroke patients treated with thrombolysis.

BACKGROUND: Elevated levels of cardiac troponin T (cTnT) have been associated with unfavorable outcomes in cardiac patients. However, no studies, to date, have discussed the prognostic value of high-sensitivity cTnT (hs-cTnT) in thrombolyzed patients with acute ischemic stroke (AIS). HYPOTHESIS: We hypothesized that elevated levels of hs-cTnT would be associated with poorer clinical outcomes in AIS patients treated with intravenous tissue-type plasminogen activator (IV tPA). METHODS: From January 2017 to February 2018, a total of 241 AIS patients treated with IV tPA within 4.5 hours of onset were recruited. On admission, patients were stratified into either normal or elevated hs-cTnT groups according to a cutoff value of 14 ng/L. Multivariable logistic regression analyses were conducted to identify determinants of hs-cTnT elevation and to detect whether elevated hs-cTnT was associated with disability and/or mortality. RESULTS: In multivariable regression analysis, older age (P < .001) and stroke etiology (P = .024) were significantly associated with elevated hs-cTnT levels. After adjusting for demographic and clinical characteristics, hs-cTnT elevation was still significantly associated with 14-day major disability (modified Rankin Scale (mRS) 3-5, model 1, P = .019, odds ratio [OR] 2.677; model 2, P = .015, OR 2.834), 14-day composite unfavorable outcome (mRS 3-6, model 1, P = .005, OR 3.525; model 2, P = .003, OR 3.976), 30-day mortality (P = .049, OR 4.545) and 90-day mortality (P = .049, OR 3.835). CONCLUSIONS: Elevation of hs-cTnT at admission is associated with an increased risk of 90-day mortality in AIS patients treated with IV tPA.

The critical interaction between valproate sodium and warfarin: case report and review.

BACKGROUND: Valproic acid (VPA) and warfarin are commonly prescribed for patients with epilepsy and concomitant atrial fibrillation (AF). When VPA and warfarin are prescribed together, clinically important interactions may occur. VPA may replace warfarin from the protein binding sites and result in an abnormally increased anticoagulation effect. This is commonly underrecognized. CASE PRESENTATION: In our case, we report a 78-year-old woman with a glioma who presented with status epilepticus. The patient was on warfarin to prevent cardiogenic embolism secondary to AF. Intravenous loading dose of VPA was administered, but international normalized ratio (INR) increased significantly to 8.26. Intravenous vitamin K1 was then given and the patient developed no overt bleeding during the hospitalization. CONCLUSION: By reviewing the literature and discussing the critical interaction between valproate sodium and warfarin, we conclude that intravenous VPA and the co-administrated warfarin may develop critical but underrecognized complications due to effects on the function of hepatic enzymes and displacement of protein binding sites.

Oxymatrine inhibits collagen synthesis in keloid fibroblasts via inhibition of transforming growth factor-ß1/Smad signaling pathway.

BACKGROUND: Keloids are benign dermal tumors characterized by fibroblastic proliferation and excessive accumulation of collagen. Oxymatrine (OMT) is an alkaloid extracted from the Chinese herb Sophora japonica with capacities of anti-fibrosis. OBJECTIVE: To evaluate the effects of OMT on collagen production and to explore its mechanisms. METHODS: OMT was applied to human keloid fibroblasts in vitro. Collagen, transforming growth factor (TGF)-ß1, TGF-ß receptor, and Smads were analyzed by Western Blot, reverse transcription polymerase chain reaction, and immunofluorescence. RESULTS: We found that both collagen synthesis and Smad3 production were significantly suppressed in a dose-dependent administration of OMT. However, expression of TGF-ß1, TGF-ß receptor1, TGF-ß receptor2, Smad4, and Smad7 was unchanged. We also found that OMT reversed phosphorylation and nuclear translocation of Smad3 induced by TGF-ß1. CONCLUSIONS: OMT inhibited collagen synthesis, which might be associated with TGF-ß/Smad signaling pathway. These findings suggest that OMT may be a promising candidate to prevent keloid and other fibrotic diseases.

Neural cell injury microenvironment induces neural differentiation of human umbilical cord mesenchymal stem cells.

This study aimed to investigate the neural differentiation of human umbilical cord mesenchymal stem cells (hUCMSCs) under the induction of injured neural cells. After in vitro isolation and culture, passage 5 hUCMSCs were used for experimentation. hUCMSCs were co-cultured with normal or Aß1-40-injured PC12 cells, PC12 cell supernatant or PC12 cell lysate in a Transwell co-culture system. Western blot analysis and flow cytometry results showed that choline acetyltransferase and microtubule-associated protein 2, a specific marker for neural cells, were expressed in hUCMSCs under various culture conditions, and highest expression was observed in the hUCMSCs co-cultured with injured PC12 cells. Choline acetyltransferase and microtubule-associated protein 2 were not expressed in hUCMSCs cultured alone (no treatment). Cell Counting Kit-8 assay results showed that hUCMSCs under co-culture conditions promoted the proliferation of injured PC12 cells. These findings suggest that the microenvironment during neural tissue injury can effectively induce neural cell differentiation of hUCMSCs. These differentiated hUCMSCs likely accelerate the repair of injured neural cells.