Downregulation of lncRNA H19 sensitizes melanoma cells to cisplatin by regulating the miR-18b/IGF1 axis.

Long noncoding RNAs (LncRNAs) lncRNA H19 has been shown to be involved in the chemotherapy resistance of cancer cells. However, the role of lncRNA H19 in chemotherapy resistance of melanoma cells remains unknown. Here, we determined lncRNA H19, miR-18b, and insulin-like growth factor 1 (IGF1) expression by utilizing quantitative real-time PCR. Cell proliferation ability and chemosensitivity were assessed by colony formation assay and MTT assay. Flow cytometry assay was applied to detect cell apoptosis. We discovered that lncRNA H19 was upregulated, but miR-18b was downregulated in melanoma tissues and cisplatin (DDP)-resistant melanoma cells. The overall survival for the group with lower lncRNA H19 was significantly better than the group with higher H19. IGF1 mRNA level was higher in melanoma tissues than that in normal tissues. miR-18b expression level A negative correlation was observed between the expression levels of miR-18b, lncRNA H19, and IGF1 mRNA. Functionally, knockdown of lncRNA H19 sensitized resistant A375/DDP and M8/DDP cells to DDP. Silencing lncRNA H19 inhibited colony formation ability and promoted apoptosis of DDP-resistant melanoma cells, which was abrogated by miR-18b inhibition and IGF1 upregulation. Mechanistically, lncRNA H19 directly interacted with miR-18b to regulate its expression. IGF1 was identified as a target of miR-18b. These findings highlight the fact that lncRNA H19 could influence DDP-resistance by modulating the miR-18b/IGF axis in melanoma cells, suggesting a new potential therapeutic target for melanoma patient treatment.

Unexplained infertility patients have increased serum IL-2, IL-4, IL-6, IL-8, IL-21, TNFα, IFNγ and increased Tfh/CD4 T cell ratio: increased Tfh and IL-21 strongly correlate with presence of autoantibodies.

Infertility is a disease of the reproductive system that affects millions of people globally. Reproductive failure is a major medical issue adversely affecting human health in the 21st century. Many factors contribute to infertility, including immune conditions which may lead to immune infertility (immunologic infertility). It is known that specific T helper cells (Th) and their cytokines are involved in the stages of infertility. The aim of this study is to provide a new diagnostic approach to immunologic infertility by investigating the correlation of follicular helper T cells (Tfh) and their secreted cytokines with the autoantibodies in peripheral blood samples from immunologically infertile patients. Thirty (30) patients suffering from immune infertility and 20 control subjects were selected as the sample base for this study. The levels of Tfh, 20 cytokines and 4 antibodies were evaluated for this investigation and evaluated using flow cytometry, antibody chip and ELISA technologies. It was found that, in immunologically infertile patients, Tfh cell numbers were significantly higher than those in the control group. Likewise, seven (7) serum cytokines were expressed to a greater degree in infertile patients compared to the control group. Finally, four (4) antibodies were found to be higher in immunologically infertile patients. The results show that, among patients with immunologic infertility, the levels of Tfh cells and IL-21 were increased significantly in peripheral blood samples and correlate positively with the autoantibodies. IL-12 was positively correlated with the two antibodies, while TNFα was negatively correlated with two additional antibodies. The detection and quantification of Tfh cells, IL-21, IL-12 and TNFα may provide new diagnostic indicators to screen for immunologic infertility.

Prognostic utility of gene therapy with herpes simplex virus thymidine kinase for patients with high-grade malignant gliomas: a systematic review and meta analysis.

The aim of this study was to assess the effectiveness of adding viral vector-mediated gene therapy with herpes simplex virus thymidine kinase (HSV-tk) to standard treatment, in comparison with standard treatment alone to treat patients with high-grade gliomas (HGGs). A literature search of the databases PubMed, Embase, the Cochrane Library, Web of Science, and Chinese biomedicine was performed to identify eligible studies. Three randomized controlled trials (involving a total of 532 patients) were included in this systematic review. A meta-analysis of included studies demonstrated a significant increase in median survival time (MST) in patients who were treated with HSV-tk gene therapy (mean deviation 0.59, 95% CI: 0.41-0.76, p < 0.0001). The results of pooled analysis for different patient groups show that overall survival (OS) for all HGG patients was improved by adding gene therapy [hazard ratio (HR) = 0.91, 95% CI: 0.74-1.13, p = 0.42], while a different result was seen for glioblastoma multiforme (GBM) patients (HR = 1.06, 95% CI: 0.80-1.41, p = 0.70). Furthermore, the combined results for tumor progression implied that standard therapy was superior to gene therapy [odds ratio (OR) = 1.31, p = 0.09]; yet differences in HR and OR between experimental groups and control groups had no statistical significance (p > 0.05). Based on the best available evidence, it appears that adding gene therapy with HSV-tk has some effect in treating HGG patients, especially with respect to MST. However, neither the pooled analysis of OS, nor the combined analysis of tumor progress indicates any significant advantage to adding gene therapy compared with standard treatment alone. More prospective studies are needed to draw solid conclusions about whether gene therapy has significant prognostic advantage.

Association between DNA repair genes (XPD and XRCC1) polymorphisms and susceptibility to age-related cataract (ARC): a meta-analysis.

BACKGROUND: DNA repair gene (XPD and XRCC1) polymorphisms have been considered as risk factors for the development of age-related cataract (ARC). To confirm the association between DNA repair gene (XPD and XRCC1) polymorphisms and the risk of ARC, a meta-analysis was conducted. METHODS: A search was made of published literature from Institute for Scientific Information (ISI) Web of Knowledge, PubMed, Google Scholar, China National Knowledge Infrastructure (CNKI), and Wanfang Data. In addition, all studies evaluating the association between DNA repair genes (XPD and XRCC1) polymorphisms and the risk for ARC were included in our analysis. Pooled odds ratio (OR) and 95 % confidence interval (CI) were calculated by using fixed- or random-effects model. The Egger's test was used to check the publication bias. RESULTS: Six studies on XRCC1 Arg399Gln (1,300 cases, 1,222 controls) and five studies on XPD Lys751Gln (1,092 cases, 1,061 controls) were included. For the XPD Lys751Gln (A/C) SNP, the overall analysis demonstrated that the CC genotype showed a significant association with a decreased risk for ARC compared with the AA genotype (OR = 0.59, 95 % CI, 0.38-0.92, P = 0.019). Similarly, the CC genotype showed a significant association with a decreased risk for ARC compared with the (AA + AC) genotype (OR = 0.65, 95 % CI, 0.43-0.98, P = 0.040). Subgroup analysis showed that the association between the CC genotype and decreased risk for ARC is statistically significant in Caucasians (OR = 0.41, 95 % CI, 0.24-0.73, P = 0.002) but not in Asians (OR = 1.06, 95 % CI, 0.51-2.19, P = 0.877). For the XRCC1 Arg399Gln (G/A) SNP, the overall analysis demonstrated that the A allele showed a significant association with an increased risk for ARC compared with the G allele (OR = 1.16, 95 % CI, 1.03-1.31, P = 0.015). Subgroup analyses exhibited that the association between the A allele and the risk for ARC was statistically significant in Asians (OR = 1.23, 95 % CI, 1.07-1.41, P = 0.003) but not in Caucasians (OR = 0.94, 95 % CI, 0.73-1.22, P = 0.660). Compared with the GG genotype, the GA genotype showed a significant association with an increased risk for ARC in Asians (OR = 1.32, 95 % CI, 1.08-1.61, P = 0.006) but not in Caucasians (OR = 0.58, 95 % CI, 0.27-1.26, P = 0.171). The Egger's test did not reveal an obvious publication bias among the included studies. CONCLUSIONS: Our meta-analysis suggested that the CC genotype of XPD Lys751Gln (A/C) SNP seemed to portend a decreased risk for ARC in Caucasian populations but not in Asian populations. The A allele and GA genotype of XRCC1 Arg399Gln (G/A) SNP might increase risk for ARC in Asian populations but not in Caucasian populations. More researches with larger and more different ethnic populations on this issue are therefore necessary.

Protective effect of isopsoralen on UVB-induced injury in HaCaT cells via the ER and p38MAPK signaling pathways.

This study investigated the protective effect of isopsoralen on UVB-induced damage in HaCaT cells and its molecular mechanism. The cytotoxicity of isopsoralen and its effects on the viability of HaCaT cells were examined using the MTT assay. The effects of UVB irradiation and isopsoralen on the intracellular glutathione (GSH-PX), superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS) content were examined using commercially available assay kits. Further, the effects of UVB irradiation and isopsoralen on the levels of the inflammatory cytokines TNF-α, IL-6, and IL-1α were examined using enzyme-linked immunosorbent assay. Finally, we examined the effect of adding the estrogen receptor (ER) antagonist ICI182780,780 and the p38MAPK antagonist SB203580 on the changes in inflammatory cytokines induced by isopsoralen treatment and UVB irradiation. Isopsoralen pretreatment markedly inhibited UVB-induced reduction in the viability and proliferation of HaCaT cells. Isopsoralen also reduced UVB-induced increase in the expression of the inflammatory cytokines and the level of free radicals (ROS and MDA), and reversed the UVB-induced suppression of antioxidant activity. Additionally, inhibition of ER and p38MAPK via the addition of their respective antagonists reversed the observed anti-inflammatory effects of Isopsoralen. Isopsoralen can efficiently provide protection against UVB-induced damage in HaCaT cells brought about via oxidation and inflammatory reactions, and the underlying mechanisms involve the ER and p38MAPK pathways. Therefore, Isopsoralen could be used in therapeutic solutions for UVB-induced skin conditions. PRACTICAL APPLICATIONS: Isopsoralen shows antioxidant and anti-inflammatory effects. As natural, healthy, and effective additives, isopsoralen has been widely used in cosmetics and botanical medicine products. The results of this study reveal the molecular mechanisms underlying isopsoralen effects, showing that isopsoralen reverses the effects of UVB irradiation regulating ER and p38MAPK signaling pathways. Consequently, isopsoralen regulates the expression of ER and p38MAPK signaling pathways, thereby reducing the activation of antioxidant and anti-inflammatory activity. These findings suggest that isopsoralen can be used as the base ingredient for antiphotoaging cosmetics and botanical medicine products. This study provides both theoretical and experimental background for isopsoralen deep processing and utilization.

lncRNA AGAP2-AS1 Facilitates Tumorigenesis and Ferroptosis Resistance through SLC7A11 by IGF2BP2 Pathway in Melanoma.

Long noncoding RNAs (lncRNAs) stand as indispensable regulators of initiation and development in melanoma (melanoma). However, the action molecular mechanisms linked to melanoma remain unclear. In the current study, the findings revealed that AGAP2-AS1 was considerably greater in melanoma than in healthy tissues and that the level of AGAP2-AS1 in cancer tissue was significantly linked to the cancerous TNM stage of patients. Individuals with high AGAP2-AS1 had a considerably shorter survival duration than patients with low AGAP2-AS1, regardless of progression-free survival or overall survival. Functionally, downregulating the expression of AGAP2-AS1 can inhibit the growth of melanocytes. Compared with the control group, AGAP2-AS1 knockdown increased Erastin-mediated iron death in melanoma cells. However, iron death inhibitor FERSINT-1 restored this effect, while Erastin induced melanoma cell death. Besides, intracellular iron and Fe2+ levels increased after AGAP2-AS1 knockdown in melanoma cells treated with Erastin compared with the si-NC group. In addition, AGAP2-AS1 silencing resulted in a significant decrease in glutathione (GSH) content in Erastin-treated melanoma cells. The mechanistic results suggest AGAP2-AS1 increases SLC7A11 mRNA stability through the IGF2BP2 pathway. In this investigation, we discovered new activities for AGAP2-AS1 and firstly discovered its mechanistic basis in ferroptosis and melanoma formation that might help in the search for potential therapy options in melanoma.

Isoastilbin inhibits neuronal apoptosis and oxidative stress in a rat model of ischemia-reperfusion injury in the brain: Involvement of SIRT1/3/6.

BACKGROUND: Isoastilbin (IAB) has been shown to have antioxidative and anti-apoptotic functions. A recent study found that IAB can reduce oxidative stress in Alzheimer's disease. However, whether the antioxidative function of IAB is also protective in other brain diseases remains unknown. OBJECTIVES: To investigate the roles and underlying mechanisms of IAB in middle cerebral artery occlusion-reperfusion (MCAO/R) in rats. MATERIAL AND METHODS: Male Wistar rats were randomly divided into 5 groups: sham group, MCAO/R group, and 3 MCAO/R groups groups administered IAB (20 mg/kg, 40 mg/kg or 80 mg/kg) once a day for 3 days. Infarction size, modified Neurological Severity Score (mNSS), oxidative stress markers, and neuronal apoptosis markers were used to assay the function of IAB. RESULTS: Compared with the MCAO/R group, administration of IAB reduced the infarction size and mNSS scores in MCAO/R rats. Isoastilbin also decreased the level of malondialdehyde (MDA) and enhanced the activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). Isoastilbin treatment attenuated MCAO/R-induced neuronal apoptosis compared with the MCAO/R group, as indicated by the results of terminal deoxynucleotide transferase-mediated X-dUTP nick end (TUNEL) and western blot assays. Isoastilbin also reversed MCAO/R-induced downregulation of SIRT1/3/6 protein expression. CONCLUSIONS: These observations suggest that IAB protects against oxidative stress and neuronal apoptosis in rats following cerebral ischemia-reperfusion (I/R) injury through the upregulation of SIRT1/3/6, indicating that IAB might be a promising therapeutic agent for cerebral I/R injury.

Protective Effect of Schisandrin on CORT-Induced PC12 Depression Cell Model by Inhibiting Cell Apoptosis In Vitro.

Background: In recent years, the incidence of depression is on the rise. Our paper proposed to study the protective effects of Schisandrin on CORT-induced PC12 depressive cell model and the underlying mechanisms. Methods: The in vitro models of PC12 were established using corticosterone (CORT). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method was used to screen the effective concentration of Schisandrin, and the models of PC12 were treated with low, medium, and high concentrations of Schisandrin. The cell activity of each group was detected by MTT assay. The LDH activity in each group of cells was detected by lactate dehydrogenase (LDH) kit. Apoptosis rate of each group was detected by Annexin V-FITC apoptosis assay kit. Mitochondrial membrane potential of each group of cells was detected by mitochondrial membrane potential kit. The protein expression levels of Caspase-3, Bax, and Bcl-2 in each group of cells were detected by western blot. Results: The treatment of Schisandrin significantly increased the cell viability in models of PC12. In addition, the results of LDH activity suggested that Schisandrin significantly reduced LDH content in models of PC12. Consistently, Schisandrin reduced the mitochondrial membrane potential of CORT-induced PC12 depressive cell model. Furthermore, Schisandrin effectively reduced the number of apoptotic cells and inhibited the expression of proapoptotic-related proteins (cleaved Caspase-3 and Bax) but increased the antiapoptotic-related protein (Bcl-2) in the models of PC12. Conclusions: Protective effects of Schisandrin on CORT-induced PC12 depressive cell model by inhibiting cells apoptosis in vitro.

Protective effect of effective part of Acanthopanacis senticosus on damage of PC12 cells induced by MPP+.

The purpose of our research was to evaluate the protective effect of the effective part of Acanthopanacis senticosus (AS) on the damage of PC12 cells induced by MPP+, an in vitro cell model for Parkinson's disease. Cell viability and apoptosis of PC12 cells induced by MPP' were assayed by MTT and flow cytometry respectively in the presence or absence of the effective part of AS. The contents of lactate dehydrogenase (LDH), nitric oxide (NO), nitric oxide synthase (NOS) and malondialdehyde (MDA) were determined by UV spectrophotometer. Our study showed that the survival rate of PC12 cells was markedly increased while cell apoptosis was decreased in the range of 200 to 400 mg x L(-1) of the effective part of AS. The contents of LDH, NO, NOS, MDA were reduced. Our experimental results indicated that the effective part of AS had the protective effect on the damage of PC12 cells induced by MPP+. The underlying mechanisms might be the combination of reduction of LDH leakage and decreases in the contents of NO, NOS and MDA, and finally prevent the apoptosis in PC12 cells and increase the cell survival rate.

Pharmacological Effects of Novel Peptide Drugs on Allergic Rhinitis at the Small Ribonucleic Acids Level.

Using an allergic rhinitis (AR) model, we evaluated the pharmacological effects of novel peptide drugs (P-ONE and P-TWO) at the small RNA (sRNA) level. Using high-throughput sequencing, we assessed the sRNA expression profile of the negative control, AR antagonist (positive control), P-ONE, and P-TWO groups. By functional clustering and Gene Ontology and KEGG pathway analyses, we found that sRNA target genes have a specific enrichment pattern and may contribute to the effects of the novel peptides. Small RNA sequencing confirmed the biological foundations of novel and traditional AR treatments and suggested unique pharmacological effects. Our findings will facilitate evaluation of the pathogenesis of AR and of the pharmacological mechanisms of novel peptide drugs.

P-FN12, an H4R-Based Epitope Vaccine Screened by Phage Display, Regulates the Th1/Th2 Balance in Rat Allergic Rhinitis.

Allergic rhinitis (AR) involves antigen-specific immune-inflammation of the nasal mucosa. Classical therapy for AR targets the histamine pathway, e.g., histamine receptor blockers. Histamine H4 receptor (H4R) was suggested as a novel therapeutic target due to its wide expression on almost all immune-related cells. A 12-mer random peptide library was used to select the specific epitope of the H4R. The phage clone showing the highest degree of activation was verified and translated to the corresponding peptide. The peptide FNKWMDCLSVTH, designated as P-FN12, was bound by H4R monoclonal antibody (mcAb) with high affinity. Moreover, the P-FN12 + CTB@Lipo-formulated vaccine, used as nasal drops, decreased allergic symptoms such as sneezing and nasal rubbing in a rat model. The level of ovalbumin (OVA)-specific immunoglobulin E (IgE) decreased significantly after vaccine administration. It also elicited increased levels of interferon (IFN)-γ and interleukin-2 (IL-2) but a decreased level of IL-4, and it elevated the T helper type 1 (Th1):T helper type 2 (Th2) cell ratio in peripheral blood mononuclear cell cultures. Our results indicated that the reduction of allergic inflammation by P-FN12-based vaccine was related to a decrease in production of OVA-specific IgE, Th2 immunity, and tissue eosinophilia. P-FN12 + CTB@Lipo is a promising vaccine that could suppress Th2 response and enhance the induction of Th1 cells in an AR model.

Advances in recurrence and malignant transformation of sinonasal inverted papillomas.

Sinonasal inverted papilloma (SIP) is a benign tumor of the nasal cavity and sinus. SIP is characterized by aggressive malignant transformation and a high rate of recurrence. Inadequate removal of the tumor during surgery is one of the most significant contributors to SIP recurrence. A growing body of evidence suggests that molecular alteration in SIP, including human papilloma virus infections, single nucleotide polymorphisms of key genes, deregulation of signaling pathways and immunological changes, may lead to SIP occurrence and malignant transformation. However, the extent to which these molecular mechanisms contribute to SIP pathology and transformation remains unclear due to limited research. Further studies are warranted to elucidate the primary dependent factors that contribute to SIP etiology. The present article reviewed risk factors of progression and recurrence of SIP, including outdoor and industrial occupational exposure, smoking, septal deviation, SIP location, recurrent cases, stage of SIP-associated squamous cell carcinoma and choice of surgical method.

A network-based method using a random walk with restart algorithm and screening tests to identify novel genes associated with Menière's disease.

As a chronic illness derived from hair cells of the inner ear, Menière's disease (MD) negatively influences the quality of life of individuals and leads to a number of symptoms, such as dizziness, temporary hearing loss, and tinnitus. The complete identification of novel genes related to MD would help elucidate its underlying pathological mechanisms and improve its diagnosis and treatment. In this study, a network-based method was developed to identify novel MD-related genes based on known MD-related genes. A human protein-protein interaction (PPI) network was constructed using the PPI information reported in the STRING database. A classic ranking algorithm, the random walk with restart (RWR) algorithm, was employed to search for novel genes using known genes as seed nodes. To make the identified genes more reliable, a series of screening tests, including a permutation test, an interaction test and an enrichment test, were designed to select essential genes from those obtained by the RWR algorithm. As a result, several inferred genes, such as CD4, NOTCH2 and IL6, were discovered. Finally, a detailed biological analysis was performed on fifteen of the important inferred genes, which indicated their strong associations with MD.

Identifying novel genes and chemicals related to nasopharyngeal cancer in a heterogeneous network.

Nasopharyngeal cancer or nasopharyngeal carcinoma (NPC) is the most common cancer originating in the nasopharynx. The factors that induce nasopharyngeal cancer are still not clear. Additional information about the chemicals or genes related to nasopharyngeal cancer will promote a better understanding of the pathogenesis of this cancer and the factors that induce it. Thus, a computational method NPC-RGCP was proposed in this study to identify the possible relevant chemicals and genes based on the presently known chemicals and genes related to nasopharyngeal cancer. To extensively utilize the functional associations between proteins and chemicals, a heterogeneous network was constructed based on interactions of proteins and chemicals. The NPC-RGCP included two stages: the searching stage and the screening stage. The former stage is for finding new possible genes and chemicals in the heterogeneous network, while the latter stage is for screening and removing false discoveries and selecting the core genes and chemicals. As a result, five putative genes, CXCR3, IRF1, CDK1, GSTP1, and CDH2, and seven putative chemicals, iron, propionic acid, dimethyl sulfoxide, isopropanol, erythrose 4-phosphate, ß-D-Fructose 6-phosphate, and flavin adenine dinucleotide, were identified by NPC-RGCP. Extensive analyses provided confirmation that the putative genes and chemicals have significant associations with nasopharyngeal cancer.

[Research on resveratrol's effects on suppressing growth and inducing apoptosis of GBC cells].

OBJECTIVE: To explore the contribution of resveratrol (Res) to the proliferation and apoptosis of gallbladder carcinoma (GBC) cell line as well as fibroblast 3T3 cell line in vitro. METHODS: The tumor cell growth repressing rate was measured by the MTT method,and flow cytometry was used to analyse cell cycle. The gene expression of bcl-2 c-myc p53 were examined by SABC. RESULTS: Res obviously suppressed the proliferation (P <0. 01) in concentration and time dependent manner, it's tiptop was 54%. Res could induce apoptosis of tumor cells. The maximum apoptosis rate of tumor was 30. 52%, experiment group compared with comparison group Gl's cells rised from 34. 88% to 55.47 +/- 3. 95%, S's cells reduced 8.41 - 17.54%, which showed obvious phenomenon of G0/G1 blocking. The GBC cell's bcl-2, c-myc gene reduced expression,while p53 gene increased expression. CONCLUSION: The results of this study confirm the ability of Res to suppress the proliferation of gallbladder carcinoma (GBC) cell with a typical apoptotic feature in vitro. Therefore, Res may be considered as a possible treatment strategy for gallbladder carcinoma.

[Sudden deafness as the initial manifestation of chronic myelogenous leukemia: case report].

To study the pathogenesis of hearing loss in chronic myelogenous leukemia (CML). To report one case with CML whose first sign was sudden unilateral hearing loss. Sudden hearing loss in CML was presented with dramatic high white blood cell count in peripheral blood. Some cases of sudden hearing loss in CML may be improved or even cured by leukapheresis and intrathecal chemotherapy. The proposed pathogenesis for deafness in leukemia is due to hyperleukocytosis, hyperviscosity syndrome, leukemic infiltration and the inner ear hemorrhage. In treatment, clinicians should quickly reduce the number of white blood cells to lighten the tumor burden. Intrathecal injection of MTX and plasmapheresis is commonly used.

[Allergic inflammation in respiratory system].

The pathophysiology of allergic disease such as asthma and allergic rhinitis tell the similar story: when the endogenous and exogenous inflammatory mechanisms occur disorder, the body may begin with inflammatory cell activation, namely through the release of cytokine and inflammatory mediator role in the corresponding target cells, activate the sensory nerve fiber, acting on the cell organ specificity effect, clinical symptoms. This article is divided into the following five parts focused on the research progress of allergic inflammatory diseases: (1) inflammatory cells; (2) staphylococcus aureus superantigen; (3) small molecules (cytokines, inflammatory mediators, lipid classes medium); (4) nerve fibers and effect cells; (5) genetic and epigenetic factors.

[Etiologies, treatment and prognosis of olfactory dysfunction].

Olfaction is one of the ancient sensing capabilities and plays an important role in monitoring environment. Although olfactory loss is common, it's obviously underappretiated by medical community generally. In order to help patients with those problems, the author gives an brief review about the characters of common etiologies, treatment and prognosis of Olfactory Dysfunction. It's concluded that most usual causes resulting in dysos- mia are upper-respiratory-tract infections, trauma, and chronic rhinosinusitis; and our understanding of the olfaction mechanism grows, but frustratingly, aside from the possible therapeutic potential of systemic steroids, no method has been proved to have solid evidence for curing olfactory loss; so we need more new basic and clinic research to develop effective therapeutic intervention.

The expression and significance of immunoglobulin free light chain in the patients with allergic rhinitis and nonallergic rhinitis.

BACKGROUND: Inflammation has been shown to be an integral component of allergic rhinitis (AR). However, there is no noteworthy debate regarding this fact in nonallergic rhinitis (NAR). Some studies have suggested that exclusion of inflammation is indicative of NAR and other studies have indicated that most of the NAR patients have some degree of inflammation. Recently, it has been shown that the level of immunoglobulin free light chains (IgFLCs) in serum is increased in some autoimmune diseases and airway inflammation. This study was designed to show whether IgFLC is associated with non-IgE-mediated rhinitis to reveal the relationship between the expression of IgFLC and activation of mast cells and eosinophils. METHODS: Thirty patients with IgE-mediated AR and 30 patients with NAR and 30 healthy persons as control were involved this study. The total IgE, IgFLC, eosinophil cationic protein (ECP) and mast cell tryptase (MCT) in serum, and nasal secretions were assayed, respectively. For identifying the expression cells of IgFLC in nasal mucosa, the immunohistochemical (IHC) staining for kappa-FLC, gamma-FLC, ECP, and MCT were performed on 30 specimens. Meanwhile, the mRNA expression of kappa-FLC, gamma-FLC, and MCT was determined by real-time quantitative polymerase chain reaction. RESULTS: IgFLCs (kappa/lambda) levels in serum and nasal secretion were significantly increased in AR patients and NAR patients. The ECP and MCT levels in serum and nasal secretion were significantly enhanced in AR and NAR patients when compared with healthy control subjects (p < 0.01). There was a positive correlation between IgFLC (kappa/lambda) and MCT in nasal secretion of patients with NAR, but only IgFLC (kappa-FLC was associated with MCT in AR. There was no correlation between IgFLC and ECP in nasal secretion. In serum expression level, there was a positive correlation between IgFLC (kappa) and ECP in AR or IgFLCs (lambda) and ECP in NAR. IHC staining showed that FLC(+) cells were significantly increased in AR and NAR mucosa, kappa-FLC was mainly expressed in epithelial cells, and lambda-FLC was mainly expressed in subepithelial cells. Double immunofluorescence staining showed that the expression of lambda-FLC was mainly localized in mast cells in NAR nasal mucosa (45%). CONCLUSION: These findings suggest strongly that IgFLC may play an important role in inducing local nasal mucosa inflammation especially those in AR and NAR.