Evaluation of gustatory and olfactory function among premenopausal and postmenopausal women and men

BACKGROUND AND AIM: The sense of taste is a chemical sense which allows everyone to perceive the flavor of what is eaten or drunk. Also, the sense of olfaction is also a chemical sense contributing to the sense of taste to perceive the taste and flavor of food. In the present work, the gustatory and olfactory function in pre- and postmenopausal women and men were studied and compared to each other. METHODS: Fifty postmenopausal women, 50 age-matched men, 50 young women and 50 young men were evaluated in this study and enrolled through simple sampling method. The aim of this study was explained for patients and in case of their consent, they were given the questionnaire. Taste threshold for each of the four main tastes for all of the participants in the study was determined at one step between 8 am to 11 am while they had not consumed any food since one hour before the test. The whole mouth taste method was used in this study. Also, the Davidson and Murphy tests were performed and the quality identification and intensity ratings of olfaction were measured. RESULTS: Three individuals among the postmenopausal women group and 2 old men were not able to detect sweet taste even in high concentration; in the group of young men, one man was not able to detect bitter taste even in high concentration. This study showed that 2% of postmenopausal women and 4% of matched men were not able to detect the odor of isopropanol even at a concentration of 70% and there was a significant relationship between odor perception of isopropanol and olfactory intensity between the two groups of pre- and postmenopausal women as well as men. CONCLUSION: Taste dysfunction directly influences nutritional status. In this study, the strength of the sweet taste perception was significantly lower among women after menopause; however, there was no significant difference between the perception of other tastes among postmenopausal women and men of same age. KEYWORDS: Taste; Olfactory; Menopaus

Ameloblastic fibro-odontoma: A case report

BACKGROUND AND AIM: Ameloblastic fibro-odontoma (AFO) is a rare, mixed odontogenic tumor that usually occurs in children and young adults with no gender predominance. Posterior mandibular region is usually involved and a painless swelling is the most common clinical feature. CASE REPORT:We here report a case of AFO in a 12-year-old girl with a complaint of a painful expansive lesion in the right posterior mandible. Radiographic examination showed a well-defined radiolucency containing radiopaque materials. The second molar was displaced by the lesion. Enucleation was conducted and no recurrence was observed after 4 years of follow-up. CONCLUSION: AFO is a benign expansive jaw lesion which develops in children. To treat AFO, proper surgical excision and curettage should be performed. KEYWORDS: Ameloblastic Fibro-Odontoma; Odontogenic Tumors; Neoplas

The theory of mind among deaf children: a review of the Theoretical Foundations

The ability to understand that others have mental states such as thoughts, tendencies, and beliefs that can be different from one's own mental state or reality is called the "theory of mind". In this article, we will first try to explain the theoretical foundations of what is now known as the theory of mind, and then, by reviewing research published on the development of the theory of mind in deaf children, we seek to research the theory of mind about hearing impaired children. Some theorists believe that the growth of the theory of mind is dependent on linguistic experience, in contrast to theorists who believe that the growth of the theory of mind is related to an executive function. Some researches have shown that latent deafness has succeeded in achieving mental theory. On the other hand, studies have shown that there is no delay in the theory of the minds of deaf children

A multifactorial role for P. falciparum malaria in endemic Burkitt\u27s lymphoma pathogenesis

Endemic Burkitt\u27s lymphoma (eBL) arises from the germinal center (GC). It is a common tumor of young children in tropical Africa and its occurrence is closely linked geographically with the incidence of P. falciparum malaria. This association was noted more than 50 years ago. Since then we have learned that eBL contains the oncogenic herpes virus Epstein-Barr virus (EBV) and a defining translocation that activates the c-myc oncogene. However the link to malaria has never been explained. Here we provide evidence for a mechanism arising in the GC to explain this association. Accumulated evidence suggests that eBL arises in the GC when deregulated expression of AID (Activation-induced cytidine deaminase) causes a c-myc translocation in a cell latently infected with Epstein-Barr virus (EBV). Here we show that P. falciparum targets GC B cells via multiple pathways to increase the risk of eBL. 1. It causes deregulated expression of AID, thereby increasing the risk of a c-myc translocation. 2. It increases the number of B cells transiting the GC. 3. It dramatically increases the frequency of these cells that are infected with EBV and therefore protected from c-myc induced apoptosis. We propose that these activities combine synergistically to dramatically increase the incidence of eBL in individuals infected with malaria

Strength and weakness of the National Nutrition Improvement Program in Rural and Nomadic Women: findings from a policy triangle framework

IntroductionNutrition-sensitive agriculture (NSA) is a comprehensive, inter-sectoral approach to improve food security and nutrition. In Iran, “National Nutrition Improvement Program in Rural and Nomadic Women” has been developed and implemented as a NSA program. The main purpose of this study was analysis of this program using the Policy Triangle Framework.MethodsThis was a qualitative policy analysis study, which was conducted retrospectively. The study population included policymakers and executors at macro (Tehran Province) and micro levels (County and village) from the two involved ministries, as well as rural women in Tehran province. The collected data included the program document (N = 210), in-depth semi-structured interviews (N = 40), as well as focus group discussions (N = 8). Data was analyzed using MAXQDA 2010 software with a deductive approach.ResultsThe findings of this study indicated that the underlying factors including social, economic and cultural status, health, structural-environmental and political are associated to the development of the program. The current program is a multi-faceted, in accordance with the existing needs, which provides opportunities to improve nutrition and community health, empower women, strengthen socio-economic status at the micro and macro levels and pave the way for other projects, by connecting the nutrition sector to agriculture. The analysis has also shown that the content of this program requires more consideration in budget and motivational measures. Although developing an NSA program based on inter-sectoral collaboration is a valuable step, it needs to be improved in the areas of sustainability, inter-sectoral collaboration, resources and facilities, monitoring and evaluation, as well as needs assessment.ConclusionThe findings of the present study can be used as evidence by policymakers and planners in redesigning and implementing the program, or developing other NSA programs

Bacterial RNA:DNA hybrids are activators of the NLRP3 inflammasome

Enterohemorrhagic Escherichia coli (EHEC) is an extracellular pathogen that causes hemorrhagic colitis and hemolytic uremic syndrome. The proinflammatory cytokine, interleukin-1beta, has been linked to hemolytic uremic syndrome. Here we identify the nucleotide-binding domain and leucine rich repeat containing family, pyrin domain containing 3 (NLRP3) inflammasome as an essential mediator of EHEC-induced IL-1beta. Whereas EHEC-specific virulence factors were dispensable for NLRP3 activation, bacterial nucleic acids such as RNA:DNA hybrids and RNA gained cytosolic access and mediated inflammasome-dependent responses. Consistent with a direct role for RNA:DNA hybrids in inflammasome activation, delivery of synthetic EHEC RNA:DNA hybrids into the cytosol triggered NLRP3-dependent responses, and introduction of RNase H, which degrades such hybrids, into infected cells specifically inhibited inflammasome activation. Notably, an E. coli rnhA mutant, which is incapable of producing RNase H and thus harbors increased levels of RNA:DNA hybrid, induced elevated levels of NLRP3-dependent caspase-1 activation and IL-1beta maturation. Collectively, these findings identify RNA:DNA hybrids of bacterial origin as a unique microbial trigger of the NLRP3 inflammasome

miR-718 represses proinflammatory cytokine production through targeting phosphatase and tensin homolog (PTEN)

Bacterial sepsis involves a complex interaction between the host immune response and bacterial LPS. LPS binds Toll-like receptor (TLR) 4, which leads to the release of proinflammatory cytokines that are essential for a potent innate immune response against pathogens. The innate immune system is tightly regulated, as excessive inflammation can lead to organ failure and death. MicroRNAs have recently emerged as important regulators of the innate immune system. Here we determined the function of miR-718, which is conserved across mammals and overlaps with the 5\u27 UTR of the interleukin 1 receptor-associated kinase (IRAK1) gene. As IRAK1 is a key component of innate immune signaling pathways that are downstream of most TLRs, we hypothesized that miR-718 helps regulate the innate immune response. Activation of TLR4, but not TLR3, induced the expression of miR-718 in macrophages. miR-718 expression was also induced in the spleens of mice upon LPS injection. miR-718 modulates PI3K/Akt signaling by directly down-regulating phosphatase and tensin homolog (PTEN), thereby promoting phosphorylation of Akt, which leads to a decrease in proinflammatory cytokine production. Phosphorylated Akt induces let-7e expression, which, in turn, down-regulates TLR4 and further diminishes TLR4-mediated proinflammatory signals. Decreased miR-718 expression is associated with bacterial burden during Neisseria gonorrhoeae infection and alters the infection dynamics of N. gonorrhoeae in vitro Furthermore, miR-718 regulates the induction of LPS tolerance in macrophages. We propose a role for miR-718 in controlling TLR4 signaling and inflammatory cytokine signaling through a negative feedback regulation loop involving down-regulation of TLR4, IRAK1, and NF-kappaB

Relationship between thyroid stimulating hormone and metabolic syndrome in overweight/obese children

Background: Background: Obesity, especially central obesity is related to many endocrine abnormalities, such as thyroid dysfunctions. Elevated levels of thyroid stimulating hormone (TSH) is common in obese children, however, it is not clear if such condition is associated with increased cardiovascular risk factors. The study aimed to determine the association between levels of TSH in overweight and obese children with components of metabolic syndrome (Mets). Methods: The study sample included 197 overweight/obese 6-7 year old children in Tehran, Iran. Anthropometric (weight, waist circumference and height), metabolic (high-density lipoprotein cholesterol, triglycerides and fasting blood glucose) and hormonal (TSH) variables, as well as blood pressure were measured. Mets was defined according to Cook definition. Results: Totally, 20.3% and 79.7% of children were overweight and obese, respectively. Elevated levels of TSH were diagnosed in 10 subjects (5.1%), while Mets was seen in 35.4%. The most frequent component of Mets was abdominal obesity (72.5%). A weak positive correlation between BMI for age, Z scores and TSH level (r =0.11, P value= 0.123) was observed only in girls (r=0.2, P value= 0.034). TSH was not associated with components of Mets. Conclusion: Elevated TSH levels may be found in obese children; however, the association between TSH elevation and cardiovascular disease risk factors, including components of metabolic syndrome needs further investigation

CD36 coordinates NLRP3 inflammasome activation by facilitating the intracellular nucleation from soluble to particulate ligands in sterile inflammation

Particulate ligands including cholesterol crystals and amyloid fibrils induce NLRP3-dependent production of interleukin-1β (IL-1β) in atherosclerosis, Alzheimer's disease and diabetes. Soluble endogenous ligands including oxidized-LDL, amyloid-β and amylin peptides accumulate in these diseases. Here we identify a CD36-mediated endocytic pathway that coordinates the intracellular conversion of these soluble ligands to crystals or fibrils, resulting in lysosomal disruption and NLRP3-inflammasome activation. Consequently, macrophages lacking CD36 failed to elicit IL-1β production in response to these ligands and targeting CD36 in atherosclerotic mice reduced serum IL-1β and plaque cholesterol crystal accumulation. Collectively, these findings highlight the importance of CD36 in the accrual and nucleation of NLRP3 ligands from within the macrophage and position CD36 as a central regulator of inflammasome activation in sterile inflammation

Interplay between Plasmodium falciparum haemozoin and l-arginine: implication for nitric oxide production

Abstract Background Plasmodium falciparum haemozoin, a detoxification product of digested haemoglobin from infected erythrocytes, is released into the bloodstream upon schizont rupture and accumulates in leukocytes. High levels of haemozoin correlate with disease severity. Some studies have shown that concentrations of the substrate of inducible nitric oxide synthase (iNOS), l-arginine, as well as nitric oxide are low in patients infected with P. falciparum malaria. The present study investigates, in vitro, the role of P. falciparum haemozoin on nitric oxide production, iNOS expression in macrophages, and the possible interaction between l-arginine and haemozoin. Methods Plasmodium falciparum haemozoin was obtained from in vitro cultures through magnetic isolation. Phagocytosis of haemozoin by immortalized bone marrow derived macrophages was detected by confocal reflection combined with fluorescence microscopy. Nitrite concentrations in the supernatants was evaluated by Griess assay as a standard indication of nitric oxide production, while iNOS expression was detected on cell extracts by western blotting. Detection of l-arginine in haemozoin-treated or untreated media was achieved by liquid chromatography–tandem mass spectrometry (LC–MS/MS). Results Haemozoin synergizes in vitro with interferon-gamma to produce nitric oxide. However, when mouse macrophages were stimulated with haemozoin, a proportional increase of nitric oxide was observed up to 25 μM of haemozoin, followed by a decrease with doses up to 100 μM, when nitric oxide release was completely abrogated. This was not due to reactive oxygen species production, nor to an effect on iNOS activity. Interestingly, when at 24 h, haemozoin-treated macrophages were washed and incubated in fresh medium for further 24 h, the nitric oxide production was restored in a dose–response manner. Similar results were seen when l-arginine-enriched media was used in the stimulation. Moreover, muramyldipeptide, a strong nitric oxide inducer, was unable to activate macrophages to release nitric oxide in the presence of haemozoin-treated medium. By LC–MS/MS a complete depletion of l-arginine was observed in this haemozoin-treated, conditioned medium. Conclusions It is proposed that haemozoin interacts with l-arginine reducing its availability for iNOS, and thus decreasing nitric oxide production. The clinical (or pathological) implications of these results are discussed