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Objective@#To explore the correlation between sleep and laryngopharyngeal reflux disease by epidemiological approaches.@*Methods@#From May 1, 2017 to April 30, 2018, data of age, gender, height, weight, smoking, alcohol consumption, constipation and high fat diet in patients in Otorhinolaryngology specialist clinic, the Eighth Medical Center, General Hospital of the Chinese PLA were retrospectively analyzed. Reflux Symptom Index (RSI), Pittsburgh Sleep Quality Index (PSQI) and Hospital Anxiety and Depression Scale (HADS)were filled. According to RSI scores, patients were divided into case group and control group. The differences of the above indicators between the two groups were compared by Stata 12.0 software, and the risk factors of LPRD were analyzed by multivariate Logistic regression.@*Results@#A total of 908 patients were enrolled, including 166 in the case group and 742 in the control group. There was no significant difference in BMI, smoking, drinking, constipation and high fat diet between the two groups (all P>0.05). The PSQI, anxiety and depression score of the case group were higher than those of the control group. The anxiety and depression scores of the patients with sleep disorders in the case group were significantly higher than those of the normal sleepers (all P<0.05). RSI of the patients with sleep disorders was higher than that of the patients with normal sleep(9.5[4.0,16.0]vs. 5.0[1.0,10.0], Z=-6.07, P<0.001). Multivariate analysis showed that sleep disorder was the risk factors of LPRD (OR=2.59, 95%CI 1.75-3.84).@*Conclusions@#Sleep disorder is related to the occurrence of LPRD. The association between LPRD and sleep disturbances is bidirectional. Sleep disorder may also be related to the anxiety and depression in LPRD patients. Handling sleep disorder timely may benefit LPRD patients.
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Objective To explore the differential expression of protein in the serum of individuals susceptible to noise induced hearing loss (NIHL) susceptible individuals working in the military tunnel.Methods A total of 40 soldiers from one tunnel construction troop were divided into the susceptible group and the nonsusceptible group.Twenty soldiers were selected for each group.The average age of the susceptible group was 24.79±2.03 years old and their thresholds of the speech and high frequencies were 22.43±8.31 dB HL and 48.55± 11.54 dB HL,respectively.The average age of the nonsusceptible group was 23.67 ± 3.56 years old and their thresholds of the speech and high frequencies were 13.40±4.13 dB HL and 9.40±2.54 dB HL,respectively.Five microliter peripheral venous blood samples were collected from each individual Two-dimensional electrophoresis (2-DE) and MALDI-TOF-MS were used to separate and identify the differentially expressed proteins.Results Thirty-seven protein spots differentially expressing between the NIHL susceptible and nonsusceptible were found after 2 DE.Compared by mascort score,10 differential proteins were harvested.Among these,5 peptides including proteasome subunit alpha-5,complement C4-A,haptoglobin,apolipoprotein A-I and vitronectin were upregulated,and other 5 ones,including Lysozyme C,beta-2 glycoprotein-1,pigment epithelium derived factor,35 kDa trypsin inhibitor heavy chain H and transthyretin were downregulated in NIHL susceptible individuals.The differences were statistically significant(P＜0.05).Conclusion The differentially expressed proteins were closely related to oxidative stress responses in susceptible individuals,including proteasome subunit alpha-5,complement C4A,haptoglobin,apolipoprotein A-I,beta-2 glycoprotein-1,pigment epithelium derived factor,35 kDa trypsin inhibitor heavy chain H and transthyretin.They might participate in the occurrence of NIHL through this way.The proteins harvested from this study were expected to be specific candidate serum NIHL susceptibility biomarkers in blood to help screen susceptible individuals.
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Objective To investigate the relationship of chronic sleep deprivation and high fat diet with laryn-gopharyngeal reflux (LPRD) .Methods A total of 16 rats were randomly divided into the experimental group and control group .Modified multiplatform water surface method and high fat diet (containing 35％ fat) were used in the experimental group rats .The rats in the control group had free sleep and normal feed .The upper gastrointestinal tract pH monitoring with double detectors was used to record the changes of pH in the both rats for 10 hours .The reflux index ,the times of re-flux with pH<4 and the longest duration of reflux were selected and converted into data of 24 hours .The three indexes of the experiment group were compared to those of the control group .Results There was no animal death during the model construction .The rats in the experimental group were irritable .There was no difference of rats weight in both groups before and after the experiment(P>0 .05) .The median of reflux index ,times of reflux with pH<4 and the longest duration of reflux of pharyngeal pH 2 detector in the rats of the experimental group were 21 .07 ,27 .25 and 61 .11 ,respectively .Those of the control group were 1 .25 ,0 .95 and 8 .44 ,respectively .Above three index of the experimental group increased obviously and the difference was statistically significant when compared to those of the control (P<0 .05) .It was suggested that LPRD might appear in the experimental group rats .The median of reflux index and the times of reflux with pH < 4 of esophageal pH1 detector in the rats of the experimental group were 15 .87 and 96 .67 ,displaying an increase when compared to those of the control group (26 .25 and 5 .6) .The differ-ences were statistically significant(P<0 .05);but the median of the longest duration of reflux in pH1 detector of the experimental group rats was 26 .25 ,failing to show statistical difference compared to that of the control group (5 .6) (P>0 .05) .Conclusion Chronic sleep deprivation and high fat diet may play an important role in the pathogenesis of LPRD .This animal model may be a new vector to study LPRD .
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Objective To investigate the number changes of the ribbon synapses(RS) in the inner hair cell of C57BL/6J mice with age .Methods The cochlear basilar membrane was obtained from C57BL/6J mice in 2 ,6 ,10 , 12 months old .RIBEYE on the presynaptic membrane and AMPA receptor on the postsynaptic membrane were double labeled by immunofluorescence histochemical technique .The stained sections were observed under a confocal laser-scanning microscope .Then the number of RS of the basilar membrane was calculated by three dimensional reconstruction images using 3DS max software .Results The numbers of RS reduced gradually from the cochlear a‐pex to base in the same developing stages .The numbers of RS in apex and middle turn of cochlea were gradually re‐duced with the age increasing .The number of RS in basilar turn reduced first and increased slowly then .Conclusion The decreases of the number of RS maybe the main pathological change at the early stage of presbycusis .In addi‐tion ,there may be a kind of compensatory mechanism by increaseing the number of RS to delay the hearing deficits .
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Objective To study the differential expression of apoptosis related genes in GJB2 gene conditional knockout mice (cCx26Pax2Cre ) cochlea membranous labyrinth ,and to explore the mechanism of GJB2 gene mutations causing deafness .Methods Two developmental stages of P10 and P18 were selected from the knock out mice and the wild type ones (BALB/C) .The total RNA was isolated from cochlear membranous labyrinth and PCR array was performed using mouse apoptosis PCR arrays .Results Compared with wild -type mice ,significant up or down -regulation in gene expression was detected in 16 genes in cCx26Pax2Cre ones at P10 .Of the 16 genes ,14 ones were down-regulated .Among the 14 genes ,9 ones can be classified as anti -apoptosis or pro -proliferation genes ,5 ones can be classified as pro -apoptosis or pro -inflammation genes .The other 2 genes expression was up-regula-ted ,and their main role was to promote apoptosis .Compared with time -matched controls ,significant up or down-regulation in gene expression was detected in 4 genes in cCx26Pax2Cre mice at P18 .Of the 4 genes ,3 ones expression was down-regulated ,were anti-apoptosis ones .The expression of the other one gene among the 4 ones was up-regulated ,which acted as pro -apoptosis genes .Bcl2l10 and Tnfrsf10b expression showed significant down or up -regulation at both stages . Compared with P10 , the expression of caspase - 8 was up - ragulated at P18 in cCx26Pax2Cre mice .Conclusion It is suggested that GJB2 mutation may up -regulate the expression of DR5 ,which can trigger the death receptor pathway to cause apoptosis in cCx 26Pax2Cre mice cochlea directly .At the same time , caspase-8 in death receptor pathway may activate the mitochondria pathway indirectly and amplify the apoptosis further in cCx26Pax2Cre mice cochlea .The final result of the above activated pathways is the wide range of cochlear cells apoptosis and the profound hearing loss in cCx 26Pax2Cre mice .