Effect of Frequency Discrimination Training on Tinnitus in Individuals with Flat Sensorineural Hearing loss.

Tinnitus is associated with sensorineural hearing loss irrespective of its severity and configuration. Frequency discrimination training is a contemporary method used for the treatment of tinnitus. However, its efficacy in treating tinnitus associated with flat sensorineural hearing loss is not studied yet. The objectives were to assess (a) treatment effect across sessions on tinnitus percept using subjective questionnaires (b) association in the severity and handicap of tinnitus before and after FDT treatment. A total of 16 participants with mean age of 56 years, who had subjective tinnitus and flat sensorineural hearing loss ranging from mild to moderate were included in the study. However, only 11 participants completed the treatment regime. Each participant was provided FDT in a game format for 15 days. The Quantitative (tinnitus pitch and loudness in each session) and qualitative measurements (THI and TFI) were assessed in each participant. Friedman test revealed a significant reduction in handicap from tinnitus as reflected in THI and reduced functionality impairment from tinnitus as reflected in TFI across sessions. Besides, a significant association was observed in the Chi-square test in severity and handicap of tinnitus before and after therapy. A change in pitch and reduced loudness was noted in eight of 11 participants. Three of them had no tinnitus perception at the end of the treatment regime. The current study findings demonstrate the efficacy of FDT using a game module in treating tinnitus associated with flat sensorineural hearing loss. The perceived severity and handicap of tinnitus reduces as a function of treatment.

miR-181c Activates Mitochondrial Calcium Uptake by Regulating MICU1 in the Heart.

Background Translocation of miR-181c into cardiac mitochondria downregulates the mitochondrial gene, mt-COX1. miR-181c/d-/- hearts experience less oxidative stress during ischemia/reperfusion (I/R) and are protected against I/R injury. Additionally, miR-181c overexpression can increase mitochondrial matrix Ca2+ ([Ca2+]m), but the mechanism by which miR-181c regulates [Ca2+]m is unknown. Methods and Results By RNA sequencing and analysis, here we show that hearts from miR-181c/d-/- mice overexpress nuclear-encoded Ca2+ regulatory and metabolic pathway genes, suggesting that alterations in miR-181c and mt-COX1 perturb mitochondria-to-nucleus retrograde signaling and [Ca2+]m regulation. Quantitative polymerase chain reaction validation of transcription factors that are known to initiate retrograde signaling revealed significantly higher Sp1 (specificity protein) expression in the miR-181c/d-/- hearts. Furthermore, an association of Sp1 with the promoter region of MICU1 was confirmed by chromatin immunoprecipitation-quantitative polymerase chain reaction and higher expression of MICU1 was found in the miR-181c/d-/- hearts. Conversely, downregulation of Sp1 by small interfering RNA decreased MICU1 expression in neonatal mouse ventricular myocytes. Changes in PDH activity provided evidence for a change in [Ca2+]m via the miR-181c/MICU1 axis. Moreover, this mechanism was implicated in the pathology of I/R injury. When MICU1 was knocked down in the miR-181c/d-/- heart by lentiviral expression of a short-hairpin RNA against MICU1, cardioprotective effects against I/R injury were abrogated. Furthermore, using an in vitro I/R model in miR-181c/d-/- neonatal mouse ventricular myocytes, we confirmed the contribution of both Sp1 and MICU1 in ischemic injury. Conclusions miR-181c regulates mt-COX1, which in turn regulates MICU1 expression through the Sp1-mediated mitochondria-to-nucleus retrograde pathway. Loss of miR-181c can protect the heart from I/R injury by modulating [Ca2+]m through the upregulation of MICU1.

The Relationship Between Acceptable Noise Level and Electrophysiologic Auditory Brainstem and Cortical Signal to Noise Ratios.

The following objectives of the study were formulated: i) to investigate differences in measured signal to noise ratios while recording speech-evoked auditory brainstem response (cABR) and cortical late latency response (LLR) in low and high acceptable noise level (ANL) groups; and ii) to compare peak to peak amplitude of cABR (V-A) and LLR (N1-P2) in low and high ANL groups. A total of 23 normal hearing participants was included in the study. One shot replicative and partly exploratory research design was utilized to study the effect of signal to noise ratio in a recorded waveform on afferent mechanism, assessed by cABR and LLR on participants having values of ANL of ≤7 (low ANL group) and ≥13 (high ANL group). There were no differences in signal to noise ratio in the recorded waveforms of cABR and LLR between low and high ANL groups at both brainstem and cortical levels. However, the peak to peak amplitude of V-A of cABR and N1-P2 of LLR were both statistically larger in the high ANL group compared to their counterpart. The signal to noise ratio in recorded waveforms did not differentiated cABR (V-A) or LLR (N1-P2) in low and high ANL groups. However, Larger peak to peak amplitudes in the high ANL group suggests differences higher processing centers in the upper brainstem to the auditory cortex. The findings of the study may be useful in determining the patient acceptability of noise.

Use of Adaptive Support Ventilation (ASV) in Ventilator Associated Pneumonia (VAP) - A Case Report.

SUMMARY: Prolonged ventilation leads to a higher incidence of ventilator associated pneumonia(VAP) resulting in ventilator dependency, increased costs and subsequent weaning failures. Prevention and aggressive treatment of VAP along with patient friendly newer modes of ventilation like adaptive support ventilation go a long way in successful management of these cases.