OBJECTIVE: This study aimed to evaluate the influence of different whitening toothpastes on color change and alteration in enamel surface roughness and microhardness compared to a conventional toothpaste.
METHODS: Fifty bovine incisors were selected, cleaned, and stored before being divided into five groups: a conventional toothpaste group (C) and three whitening toothpaste groups containing different abrasive agents: silica (S), hydrogen peroxide (PH), and activated charcoal (CA). Specimens underwent simulated brushing, staining with black tea solution, and subsequent analyses of color, surface roughness, and microhardness. Statistical analysis was performed using three-way ANOVA and Tukey post-hoc tests (P < .05).
RESULTS: The results showed that the color analysis revealed similar whitening potential among all toothpastes. Otherwise, showed significant differences in surface roughness (P < .001) and microhardness (P < .001) after simulated brushing. While all toothpastes caused a decrease in microhardness, the charcoal-based toothpaste showed a significant increase in surface roughness compared to the initial condition.
CONCLUSIONS: All toothpastes demonstrated whitening capability. Surface roughness changed after brushing with activated charcoal-based whitening toothpaste, but final roughness was similar across all groups. Whitening toothpastes led to a decrease in enamel microhardness, with similar final performance across all toothpastes analyzed.

Chlorogenic acid (CGA) is a natural polyphenol found in coffee, tea, vegetables, and fruits. It exhibits strong antioxidant activity and possesses several other biological properties, including anti-inflammatory effects, antimicrobial activity, and insulin-sensitizing properties. Moreover, it may improve lipid and glucose metabolism. This review summarizes the available information on the therapeutic effect of CGA in metabolic dysfunction-associated steatotic liver disease (MASLD). As the literature search engine, the browsers in the PubMed, Scopus, Web of Science databases, and ClinicalTrials.gov register were used. Animal trials and clinical studies suggest that CGA has promising therapeutic potential in treating MASLD and hepatic steatosis. Its mechanisms of action include antioxidant, anti-inflammatory, and anti-apoptotic effects via the activation of the Nrf2 signaling pathway and the inhibition of the TLR4/NF-κB signaling cascade. Furthermore, the alleviation of liver disease by CGA also involves other important molecules such as AMPK and important physiological processes such as the intestinal barrier and gut microbiota. Nevertheless, the specific target cell and key molecule to which CGA is directed remain unidentified and require further study.

BACKGROUND: The ketogenic diet (KD) has been highly developed in the past for the treatment of epileptic pathological states in children and adults. Recently, the current re-emergence in its popularity mainly focuses on the therapy of cardiometabolic diseases. The KD can also have anti-inflammatory and neuroprotective activities which may be applied to the prevention and/or co-treatment of a diverse range of psychiatric disorders.
OBJECTIVE: This is a comprehensive literature review that intends to critically collect and scrutinize the pre-existing research basis and clinical data of the potential advantageous impacts of a KD on stress, anxiety, depression, schizophrenia and bipolar disorder.
METHODS: This literature review was performed to thoroughly represent the existing research in this topic, as well as to find gaps in the international scientific community. In this aspect, we carefully investigated the ultimate scientific web databases, e.g., PubMed, Scopus, and Web of Science, to derive the currently available animal and clinical human surveys by using efficient and representative keywords.
RESULTS: Just in recent years, an increasing amount of animal and clinical human surveys have focused on investigating the possible impacts of the KD in the prevention and co-treatment of depression, anxiety, stress, schizophrenia, and bipolar disorder. Pre-existing basic research with animal studies has consistently demonstrated promising results of the KD, showing a propensity to ameliorate symptoms of depression, anxiety, stress, schizophrenia, and bipolar disorder. However, the translation of these findings to clinical settings presents a more complex issue. The majority of the currently available clinical surveys seem to be moderate, usually not controlled, and have mainly assessed the short-term effects of a KD. In addition, some clinical surveys appear to be characterized by enormous dropout rates and significant absence of compliance measurement, as well as an elevated amount of heterogeneity in their methodological design.
CONCLUSIONS: Although the currently available evidence seems promising, it is highly recommended to accomplish larger, long-term, randomized, double-blind, controlled clinical trials with a prospective design, in order to derive conclusive results as to whether KD could act as a potential preventative factor or even a co-treatment agent against stress, anxiety, depression, schizophrenia, and bipolar disorder. Basic research with animal studies is also recommended to examine the molecular mechanisms of KD against the above psychiatric diseases.

Diffusion tensor imaging (DTI) has emerged as a promising neuroimaging tool for detecting blast-induced mild traumatic brain injury (bmTBI). However, lack of refined acute-phase monitoring and reliable imaging biomarkers hindered its clinical application in early diagnosis of bmTBI, leading to potential long-term disability of patients. Here, we used DTI in a rat model of bmTBI generated by exposing to single lateral blast waves (151.16 and 349.75 kPa, lasting 47.48 ms) released in a confined bioshock tube (BST-I) to investigate whole-brain DTI changes in the acute-phase of bmTBI at 1, 3, 7 days after injury. Combined assessment of immunohistochemical analysis, transmission electron microscopy (TEM) and behavioral readouts allowed for linking DTI changes to synchronous cellular damages and identifying stable imaging biomarkers. The corpus callosum (CC) and brainstem were identified as predominantly affected regions, in which reduced fractional anisotropy (FA) was detected as early as the first day after injury, with a maximum decline occurring at 3 days after injury before returning to near normal levels by 7 days. Axial diffusivity (AD) values within the CC and brainstem also significantly reduced at 3 days after injury. In contrast, the radial diffusivity (RD) in the CC showed acute elevation, peaking at 3 days after injury before normalizing by the 7-day time point. Damages to nerve fibers, including demyelination and axonal degeneration, progressed in lines with changes in DTI parameters, supporting a real-time macroscopic reflection of microscopic neuronal fiber injury by DTI. The most sensitive biomarker was identified as a decrease in FA, AD and an increase in RD within the CC on the third day after injury, supporting the diagnostic utility of DTI in cases of bmTBI in the acute phase.

Steroids stand for a class of hormones (natural and synthetic) known to be helpful for a number of disorders. Despite the aforementioned beneficial effects of using these hormones, anabolic-androgenic steroids (AAS) are also widely abused in a non-therapeutic manner for muscle-building and strength-increasing properties that may lead to genotoxicity in different tissues. The present study aims to understand whether genotoxicity may be a suitable biomarker for AAS exposure in vivo in both experimental animal and human studies. All studies published in PubMed/Medline, Scopus, and Web of Science electronic databases that presented data on DNA damage caused by AAS were analyzed. A total of 15 articles were included in this study, and after thoroughly reviewing the studies, a total of 8 articles were classified as Strong, 6 were classified as Moderate, and only 1 was classified as Weak, totaling 14 studies being considered either Strong or Moderate. This classification makes it possible to consider the present findings as reliable. The meta-analysis data revealed a statistically significant difference in Wistar rat testis cells with AAS compared to control for tail length and % tail DNA (p < 0.001), so that the selected articles were considered homogeneous and the I2 of 0% indicated low heterogeneity. In summary, genotoxicity can be considered a suitable biomarker for monitoring AAS exposure as a result of DNA breakage and oxidative DNA damage.

OBJECTIVE: Paraoxonase (PON) proteins have various hydrolytic activities. The PON family is able to detoxify oxidized low-density lipoprotein. Additionally, differentiation of monocytes into macrophages, as the first stage in the development of atherosclerosis, is suppressed by PON 1. The effects of polyphenols including curcumin on PON1 have been investigated in studies. In this study, our main goal is to investigate curcumin\'s effect on PON1 protein levels, gene expression, and enzyme activity in animal interventional studies.
METHODS: The literature was searched through the online databases including PubMed, SCOPUS, Embase, and Google Scholar until May 2022.
RESULTS: Curcumin administration can increase the PON1 enzyme activity. Also, it probably has a positive role in increasing the PON1 gene expression. However, concerning the PON1 protein values, results are contradictory.
CONCLUSIONS: The findings of this study suggested positive role of curcumin in increasing PON1 enzyme activities, gene expression, and protein levels.
METHODS: Data are available from the corresponding author (Kheirouris@tbzmed.ac.ir).

Mesenchymal stem cells (MSCs) are multipotent stromal cells with the ability to self-renew and multi-directional differentiation potential. Exogenously administered MSCs can migrate to damaged tissue sites and participate in the repair of damaged tissues. A large number of pre-clinical studies and clinical trials have demonstrated that MSCs have the potential to treat the abnormalities of congenital nervous system and neurodegenerative diseases. Therefore, MSCs hold great promise in the treatment of neurological diseases. Here, we summarize and highlight current progress in the understanding of the underlying mechanisms and strategies of MSC application in neurological diseases.

Treatment therapies used to manage osteoporosis are associated with severe side effects. So worldwide herbs are widely studied to develop alternative safe & effective treatments. Cissus quadrangularis (CQ) has a significant role in bone health and fracture healing. It is documented that its extracts increase osteoblastic differentiation & mineralization. Currently, Cissus quadrangularis is available in the form of tablets in the market for oral delivery. But these conventional forms are associated with poor bioavailability. There is a need for a novel drug delivery system with improving oral bioavailability. Therefore, a Cissus quadrangularis-loaded self-emulsifying drug delivery system (CQ-SEDDS) was developed which disperses rapidly in the gastrointestinal fluids, yielding nano-emulsions containing a solubilized drug. This solubilized form of the drug can be easily absorbed through lymphatic pathways and bypass the hepatic first-pass effect. The emulsification efficiency, zeta potential, globule size, in-vitro dissolution, ex-vivo, in-vivo and bone marker studies were performed to assess the absorption and permeation potential of CQ incorporated in SEDDS. CQ-SEDDS with excipients Tween 80, Cremophor RH40, Transcutol HP & α-Tocopherol acetate had shown about 76% enhancement in the bioavailability of active constituents of CQ. This study provided the pre-clinical data of CQ-SEDDS using osteoporotic rat model studies.

Evidence suggests that neuroinflammation exhibits a dual role in the pathogenesis of major depressive disorder (MDD), both potentiating the onset of depressive symptoms and developing as a consequence of them. Our narrative review focuses on the role of the chemokine fractalkine (FKN) (also known as CX3CL1), which has gained increasing interest for its ability to induce changes to microglial phenotypes through interaction with its corresponding receptor (CX3CR1) that may impact neurophysiological processes relevant to MDD. Despite this, there is a lack of a clear understanding of the role of FKN in MDD. Overall, our review of the literature shows the involvement of FKN in MDD, both in preclinical models of depression, and in clinical studies of depressed patients. Preclinical studies (N = 8) seem to point towards two alternative hypotheses for FKN\'s role in MDD: a) FKN may drive pro-inflammatory changes to microglia that contribute towards MDD pathogenesis; or b) FKN may inhibit pro-inflammatory changes to microglia, thereby exerting a protective effect against MDD pathogenesis. Evidence for a) primarily derives from preclinical chronic stress models of depression in mice, whereas for b) from preclinical inflammation models of depression. Whereas, in humans, clinical studies (N = 4) consistently showed a positive association between FKN and presence of MDD, however it is not clear whether FKN is driving or moderating MDD pathogenesis. Future studies should aim for larger and more controlled clinical cohorts, in order to advance our understanding of FKN role both in the context of stress and/or inflammation.

With the aging of the population, the health of the elderly has become increasingly important. Postoperative cognitive dysfunction (POCD) is a common neurological complication in elderly patients following general anesthesia or surgery. It is characterized by cognitive decline that may persist for weeks, months, or even longer. Electroacupuncture (EA), a novel therapy that combines physical nerve stimulation with acupuncture treatment from traditional Chinese medicine, holds potential as a therapeutic intervention for preventing and treating POCD, particularly in elderly patients. Although the beneficial effects of EA on POCD have been explored in preclinical and clinical studies, the reliability of EA is limited by methodological shortcomings, and the underlying mechanisms remain largely unexplored. Therefore, we have synthesized existing evidence and proposed potential biological mechanisms underlying the effects of EA on neuroinflammation, oxidative stress, autophagy, the microbiota-gut-brain axis, and epigenetic modification. This review summarizes recent advances in EA and POCD, provides a theoretical foundation, explores potential molecular mechanisms for the prevention and treatment of POCD, and offers a basis for conducting relevant clinical trials.