A comparative study of glottis visualization according to the method of lifting the epiglottis in video laryngoscopy: indirect and direct lifting methods.

BACKGROUND: The direct entry of the camera under the epiglottis may provide a better view of the glottis than the indirect lifting of the epiglottis by placing the Macintosh blade tip on the vallecula when using the video laryngoscope. This study aimed to compare the efficiency of two different methods of lifting the epiglottis during the visualization of glottis using video laryngoscopy in the same patient. METHODS: This prospective study enrolled 60 patients who underwent general anesthesia with tracheal intubation. In each patient, glottic views were obtained by directly (group DE) and indirectly lifting the epiglottis (group IE). These two methods were compared using the modified Cormack and Lehane grade and the percentage of glottis opening (POGO) score as assessment parameters. RESULTS: Modified Cormack and Lehane grade showed a significant difference between the groups DE and IE (P = 0.004). The difference in the POGO score between the groups DE and IE was also statistically significant (87.5% and 64.4%, respectively; P < 0.001). CONCLUSIONS: Our results, therefore, revealed that the method of directly lifting epiglottis was better at exposing glottis than the method of indirectly lifting epiglottis using a video laryngoscope.

SAR optimization studies on a novel series of 2-anilinopyrimidines as selective inhibitors against triple-negative breast cancer cell line MDA-MB-468.

Triple-negative breast cancers (TNBCs) account for approximately 15% of breast cancer cases and exhibit an aggressive clinical behavior. In this study, we designed and synthesized two series of 2-anilinopyrimidines based on the structure of our previously reported compound 1 that act as a selective inhibitor of the basal-like TNBC cell line MDA-MB-468. Through the fine-tuning of 1, cyclic and acyclic amines at 4-position of the pyrimidine core were turned out to be crucial for the selectivity. An extensive analysis of structure-activity relationships of the analogs revealed that aminoalkyl groups at the end of the propyl chain are amenable to modification. Among the newly synthesized analogs, compound 38, bearing 4-chloropiperidinyl and cyclohexyl groups, was found to be the most potent and selective, and was about three times more potent and selective than 1 was against the TNBC cells.

Sex-specific metabolic interactions between liver and adipose tissue in MCD diet-induced non-alcoholic fatty liver disease.

Higher susceptibility to metabolic disease in male exemplifies the importance of sexual dimorphism in pathogenesis. We hypothesized that the higher incidence of non-alcoholic fatty liver disease in males involves sex-specific metabolic interactions between liver and adipose tissue. In the present study, we used a methionine-choline deficient (MCD) diet-induced fatty liver mouse model to investigate sex differences in the metabolic response of the liver and adipose tissue. After 2 weeks on an MCD-diet, fatty liver was induced in a sex-specific manner, affecting male mice more severely than females. The MCD-diet increased lipolytic enzymes in the gonadal white adipose tissue (gWAT) of male mice, whereas it increased expression of uncoupling protein 1 and other brown adipocyte markers in the gWAT of female mice. Moreover, gWAT from female mice demonstrated higher levels of oxygen consumption and mitochondrial content compared to gWAT from male mice. FGF21 expression was increased in liver tissue by the MCD diet, and the degree of upregulation was significantly higher in the livers of female mice. The endocrine effect of FGF21 was responsible, in part, for the sex-specific browning of gonadal white adipose tissue. Collectively, these data demonstrated that distinctively female-specific browning of white adipose tissue aids in protecting female mice against MCD diet-induced fatty liver disease.

Barley Sprouts Extract Attenuates Alcoholic Fatty Liver Injury in Mice by Reducing Inflammatory Response.

It has been reported that barley leaves possess beneficial properties such as antioxidant, hypolipidemic, antidepressant, and antidiabetic. Interestingly, barley sprouts contain a high content of saponarin, which showed both anti-inflammatory and antioxidant activities. In this study, we evaluated the effect of barley sprouts on alcohol-induced liver injury mediated by inflammation and oxidative stress. Raw barley sprouts were extracted, and quantitative and qualitative analyses of its components were performed. The mice were fed a liquid alcohol diet with or without barley sprouts for four weeks. Lipopolysaccharide (LPS)-stimulated RAW 264.7 cells were used to study the effect of barley sprouts on inflammation. Alcohol intake for four weeks caused liver injury, evidenced by an increase in serum alanine aminotransferase and aspartate aminotransferase activities and tumor necrosis factor (TNF)-α levels. The accumulation of lipid in the liver was also significantly induced, whereas the glutathione (GSH) level was reduced. Moreover, the inflammation-related gene expression was dramatically increased. All these alcohol-induced changes were effectively prevented by barley sprouts treatment. In particular, pretreatment with barley sprouts significantly blocked inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression in LPS-stimulated RAW 264.7. This study suggests that the protective effect of barley sprouts against alcohol-induced liver injury is potentially attributable to its inhibition of the inflammatory response induced by alcohol.

Silymarin Prevents Restraint Stress-Induced Acute Liver Injury by Ameliorating Oxidative Stress and Reducing Inflammatory Response.

Silymarin is a flavonoid extracted from the milk thistle Silybum marianum. It has been reported to prevent liver injuries induced by various chemicals or toxins. Our recent study suggested that silymarin induces hepatic synthesis of glutathione by increasing cysteine availability, which may consequently contribute to increased antioxidant capacity of the liver. In the present study, we investigated the effects of silymarin on acute liver injury induced by restraint stress. Silymarin (100 mg/kg) was orally administered to BALB/c mice every 12 h (3 times in total). After the last dose, mice were subjected to restraint stress for 6 h, and serum levels of aspartate and alanine aminotransferases, and hepatic levels of lipid peroxidation were determined. Hepatic levels of sulfur-containing metabolites such as methionine, S-adenosylmethionine, cysteine, and glutathione were also measured. The level of pro-inflammatory mediators in both liver and serum was determined. To study the mechanism of the effects of silymarin, we assessed Jun N-terminal kinase (JNK) activation and apoptotic signaling. Restraint stress induced severe oxidative stress and increased mRNA levels of pro-inflammatory mediators; both effects of restraint stress were significantly inhibited by silymarin. Moreover, administration of silymarin significantly prevented acute liver injury induced by restraint stress by blocking JNK activation and subsequently apoptotic signaling. In conclusion, these results suggest that the inhibition of restraint stress-induced liver injury by silymarin is due at least in part to its anti-oxidant activity and its ability to suppress the inflammatory response.

Misconceived Retropharyngeal Calcific Tendinitis during Management of Myofascial Neck Pain Syndrome.

Differential diagnosis of posterior neck pain is very challenging based on symptoms and physical examination only. Retropharyngeal calcific tendinitis is a rare and frequently misdiagnosed entity in various causes of neck pain. It results from calcium hydroxyapatite deposition in the longus colli muscle which is characterized by severe neck pain, painful restriction of neck movement, dysphagia, and odynophagia. We herein report a case of a patient with acute retropharyngeal calcific tendinitis, who complained of posterior neck pain, initially diagnosed and treated as a myofascial neck pain syndrome.

Surgery-first approach in class III open-bite.

Recently, surgical-orthodontic treatment without preoperative orthodontic treatment (known as the surgery-first approach or SFA) has been proposed to improve facial aesthetics from the beginning of treatment, to shorten the entire treatment period, and to take advantage of the regional accelerated phenomenon for orthodontic tooth movement. The SFA concept involves the prediction and simulation of dental alignment, incisor decompensation, and arch coordination using manual setup models. Based on this, decisions regarding the surgical movement of the maxilla and mandible can be made to correct skeletal discrepancies through manual model surgery (MMS). Although several three-dimensional (3D) virtual model surgery (VMS) programs have been introduced to reduce time-consuming manual laboratory procedures and potential errors, these programs still require three-dimensional-computed tomography data and involve complex computerized maneuvers. Because it is difficult to acquire 3D-computed tomographic scans in all cases, a 2.5-dimensional VMS program using two-dimensional lateral and posteroanterior cephalograms and 3D virtual dental models (3Txer version 2.5; Orapix, Seoul, Korea) has been introduced. In addition, because accurate prediction of postoperative orthodontic treatment is crucial for controlling dental alignment, incisor decompensation, arch coordination, and occlusal settling, a new 3D virtual orthodontic treatment system that can construct 3D virtual models, execute a 3D virtual setup, place virtual brackets at predetermined positions, and fabricate transfer jigs with customized bracket base for indirect bonding using a stereolithographic technique has also been developed. The purpose of this article was to introduce the methodology of 2.5-dimensional VMS and 3D virtual postoperative orthodontic treatment using a stereolithographic technique in SFA for a class III open-bite case.

Regulation of RCAN1 protein activity by Dyrk1A protein-mediated phosphorylation.

Two genes on chromosome 21, namely dual specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) and regulator of calcineurin 1 (RCAN1), have been implicated in some of the phenotypic characteristics of Down syndrome, including the early onset of Alzheimer disease. Although a link between Dyrk1A and RCAN1 and the nuclear factor of activated T cells (NFAT) pathway has been reported, it remains unclear whether Dyrk1A directly interacts with RCAN1. In the present study, Dyrk1A is shown to directly interact with and phosphorylate RCAN1 at Ser(112) and Thr(192) residues. Dyrk1A-mediated phosphorylation of RCAN1 at Ser(112) primes the protein for the GSK3ß-mediated phosphorylation of Ser(108). Phosphorylation of RCAN1 at Thr(192) by Dyrk1A enhances the ability of RCAN1 to inhibit the phosphatase activity of calcineurin (Caln), leading to reduced NFAT transcriptional activity and enhanced Tau phosphorylation. These effects are mediated by the enhanced binding of RCAN1 to Caln and its extended half-life caused by Dyrk1A-mediated phosphorylation. Furthermore, an increased expression of phospho-Thr(192)-RCAN1 was observed in the brains of transgenic mice overexpressing the Dyrk1A protein. These results suggest a direct link between Dyrk1A and RCAN1 in the Caln-NFAT signaling and Tau hyperphosphorylation pathways, supporting the notion that the synergistic interaction between the chromosome 21 genes RCAN1 and Dyrk1A is associated with a variety of pathological features associated with DS.