Olfactory function following open rhinoplasty: A 6-month follow-up study

<p>Abstract</p> <p>Background</p> <p>Patients undergoing any type of nasal surgery may experience degrees of postoperative olfactory dysfunction. We sought to investigate "when" the olfactory function recovers to its preoperative levels.</p> <p>Methods</p> <p>In this cohort design, 40 of 65 esthetic open rhinoplasty candidates with equal gender distribution, who met the inclusion criteria, were assessed for their olfactory function using the Smell Identification Test (SIT) with 40 familiar odors in sniffing bottles. All the patients were evaluated for the SIT scores preoperatively and postoperatively (at week 1, week 6, and month 6).</p> <p>Results</p> <p>At postoperative week one, 87.5% of the patients had anosmia, and the rest exhibited at least moderate levels of hyposmia. The anosmia, which was the dominant pattern at postoperative week 1, resolved and converted to various levels of hyposmia, so that no one at postoperative week 6 showed any such complain. At postoperative week six, 85% of the subjects experienced degrees of hyposmia, almost all being mild to moderate. At postoperative six month, the olfactory function had already reverted to the preoperative levels: no anosmia or moderate to severe hyposmia. A repeated ANOVA was indicative of significant differences in the olfactory function at the different time points. According to our post hoc Benfronney, the preoperative scores had a significant difference with those at postoperative week 1, week 6, but not with the ones at month 6.</p> <p>Conclusion</p> <p>Esthetic open rhinoplasty may be accompanied by some degrees of postoperative olfactory dysfunction. Patients need a time interval of 6 weeks to 6 months to fully recover their baseline olfactory function.</p

Genetic Polymorphisms of the Human PNPLA3 Gene Are Strongly Associated with Severity of Non-Alcoholic Fatty Liver Disease in Japanese

Nonalcoholic fatty liver disease (NAFLD) includes a broad range of liver pathologies from simple steatosis to cirrhosis and fibrosis, in which a subtype accompanying hepatocyte degeneration and fibrosis is classified as nonalcoholic steatohepatitis (NASH). NASH accounts for approximately 10-30% of NAFLD and causes a higher frequency of liver-related death, and its progression of NASH has been considered to be complex involving multiple genetic factors interacting with the environment and lifestyle.To identify genetic factors related to NAFLD in the Japanese, we performed a genome-wide association study recruiting 529 histologically diagnosed NAFLD patients and 932 population controls. A significant association was observed for a cluster of SNPs in PNPLA3 on chromosome 22q13 with the strongest p-value of 1.4 × 10(-10) (OR = 1.66, 95%CI: 1.43-1.94) for rs738409. Rs738409 also showed the strongest association (p = 3.6 × 10(-6)) with the histological classifications proposed by Matteoni and colleagues based on the degree of inflammation, ballooning degeneration, fibrosis and Mallory-Denk body. In addition, there were marked differences in rs738409 genotype distributions between type4 subgroup corresponding to NASH and the other three subgroups (p = 4.8 × 10(-6), OR = 1.96, 95%CI: 1.47-2.62). Moreover, a subgroup analysis of NAFLD patients against controls showed a significant association of rs738409 with type4 (p = 1.7 × 10(-16), OR = 2.18, 95%CI: 1.81-2.63) whereas no association was obtained for type1 to type3 (p = 0.41). Rs738409 also showed strong associations with three clinical traits related to the prognosis of NAFLD, namely, levels of hyaluronic acid (p = 4.6 × 10(-4)), HbA1c (p = 0.0011) and iron deposition in the liver (p = 5.6 × 10(-4)).With these results we clearly demonstrated that Matteoni type4 NAFLD is both a genetically and clinically different subset from the other spectrums of the disease and that the PNPLA3 gene is strongly associated with the progression of NASH in Japanese population

Absorption and mobility of foliar-applied boron in soybean as affected by plant boron status and application as a polyol complex

In the present study (i) the impact of plant Boron (B) status on foliar B absorption and (ii) the effect of B complexation with polyols (sorbitol or mannitol) on B absorption and translocation was investigated. Soybean (Glycine max (L.) Meer.) plants grown in nutrient solution containing 0 μM, 10 μM, 30 μM or 100 μM 11B labelled boric acid (BA) were treated with 50 mM 10B labelled BA applied to the basal parts of two leaflets of one leaf, either pure or in combination with 500 mM sorbitol or mannitol. After one week, 10B concentrations in different plant parts were determined. In B deficient leaves (0 μM 11B), 10B absorption was significantly lower than in all other treatments (9.7% of the applied dose vs. 26%–32%). The application of BA in combination with polyols increased absorption by 18–25% as compared to pure BA. The absolute amount of applied 10B moving out of the application zone was lowest in plants with 0 μM 11B supply (1.1% of the applied dose) and highest in those grown in 100 μM 11B (2.8%). The presence of sorbitol significantly decreased the share of mobile 10B in relation to the amount absorbed. The results suggest that 11B deficiency reduces the permeability of the leaf surface for BA. The addition of polyols may increase 10B absorption, but did not improve 10B distribution within the plant, which was even hindered when applied a sorbitol complex

Gastroesophageal reflux leads to esophageal cancer in a surgical model with mice

<p>Abstract</p> <p>Background</p> <p>Esophago-gastroduodenal anastomosis with rats mimics the development of human Barrett's esophagus and esophageal adenocarcinoma by introducing mixed reflux of gastric and duodenal contents into the esophagus. However, use of this rat model for mechanistic and chemopreventive studies is limited due to lack of genetically modified rat strains. Therefore, a mouse model of esophageal adenocarcinoma is needed.</p> <p>Methods</p> <p>We performed reflux surgery on wild-type, <it>p53</it>^{<it>A</it>135<it>V </it>}transgenic, and <it>INK4a/Arf</it>^+/-mice of A/J strain. Some mice were also treated with omeprazole (1,400 ppm in diet), iron (50 mg/kg/m, <it>i.p</it>.), or gastrectomy plus iron. Mouse esophagi were harvested at 20, 40 or 80 weeks after surgery for histopathological analysis.</p> <p>Results</p> <p>At week 20, we observed metaplasia in wild-type mice (5%, 1/20) and <it>p53</it>^{<it>A</it>135<it>V </it>}mice (5.3%, 1/19). At week 40, metaplasia was found in wild-type mice (16.2%, 6/37), <it>p53</it>^{<it>A</it>135<it>V </it>}mice (4.8%, 2/42), and wild-type mice also receiving gastrectomy and iron (6.7%, 1/15). Esophageal squamous cell carcinoma developed in <it>INK4a/Arf</it>^+/-mice (7.1%, 1/14), and wild-type mice receiving gastrectomy and iron (21.4%, 3/14). Among 13 wild-type mice which were given iron from week 40 to 80, twelve (92.3%) developed squamous cell carcinoma at week 80. None of these mice developed esophageal adenocarcinoma.</p> <p>Conclusion</p> <p>Surgically induced gastroesophageal reflux produced esophageal squamous cell carcinoma, but not esophageal adenocarcinoma, in mice. Dominant negative <it>p53 </it>mutation, heterozygous loss of <it>INK4a/Arf</it>, antacid treatment, iron supplementation, or gastrectomy failed to promote esophageal adenocarcinoma in these mice. Further studies are needed in order to develop a mouse model of esophageal adenocarcinoma.</p

Nicotinic Receptors Underlying Nicotine Dependence: Evidence from Transgenic Mouse Models.

Nicotine underlies the reinforcing properties of tobacco cigarettes and e-cigarettes. After inhalation and absorption, nicotine binds to various nicotinic acetylcholine receptor (nAChR) subtypes localized on the pre- and postsynaptic membranes of cells, which subsequently leads to the modulation of cellular function and neurotransmitter signaling. In this chapter, we begin by briefly reviewing the current understanding of nicotine's actions on nAChRs and highlight considerations regarding nAChR subtype localization and pharmacodynamics. Thereafter, we discuss the seminal discoveries derived from genetically modified mouse models, which have greatly contributed to our understanding of nicotine's effects on the reward-related mesolimbic pathway and the aversion-related habenulo-interpeduncular pathway. Thereafter, emerging areas of research focusing on modulation of nAChR expression and/or function are considered. Taken together, these discoveries have provided a foundational understanding of various genetic, neurobiological, and behavioral factors underlying the motivation to use nicotine and related dependence processes, which are thereby advancing drug discovery efforts to promote long-term abstinence

Coxiella burnetii, the Agent of Q Fever, Replicates within Trophoblasts and Induces a Unique Transcriptional Response

Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium typically found in myeloid cells. The infection is a source of severe obstetrical complications in humans and cattle and can undergo chronic evolution in a minority of pregnant women. Because C. burnetii is found in the placentas of aborted fetuses, we investigated the possibility that it could infect trophoblasts. Here, we show that C. burnetii infected and replicated in BeWo trophoblasts within phagolysosomes. Using pangenomic microarrays, we found that C. burnetii induced a specific transcriptomic program. This program was associated with the modulation of inflammatory responses that were shared with inflammatory agonists, such as TNF, and more specific responses involving genes related to pregnancy development, including EGR-1 and NDGR1. In addition, C. burnetii stimulated gene networks organized around the IL-6 and IL-13 pathways, which both modulate STAT3. Taken together, these results revealed that trophoblasts represent a protective niche for C. burnetii. The activation program induced by C. burnetii in trophoblasts may allow bacterial replication but seems unable to interfere with the development of normal pregnancy. Such pathophysiologocal processes should require the activation of immune placental cells associated with trophoblasts

Serotonin and GI Disorders: An Update on Clinical and Experimental Studies

The gastrointestinal (GI) tract is the largest producer of serotonin (5-hydroxytryptamine (5-HT)) in the body, and as such it is intimately connected with GI function and physiology. 5-HT produced by enterochromaffin (EC) cells is an important enteric mucosal signaling molecule and has been implicated in a number of GI diseases, including inflammatory bowel disease and functional disorders such as irritable bowel syndrome. This review will focus on what is known of basic 5-HT physiology and also on the emerging evidence for its novel role in activation of immune response and inflammation in the gut. Utilizing pubmed.gov, search terms such as “5-HT,” “EC cell,” and “colitis,” as well as pertinent reviews, were used to develop a brief overview of EC cell biology and the association between 5-HT and various GI disorders. It is the aim of this review to provide the readers with an update on EC cell biology and current understanding on the role of 5-HT in GI disorders specifically in inflammatory conditions