The Intelligibility of Interrupted Speech: Cochlear Implant Users and Normal Hearing Listeners

Compared with normal-hearing listeners, cochlear implant (CI) users display a loss of intelligibility of speech interrupted by silence or noise, possibly due to reduced ability to integrate and restore speech glimpses across silence or noise intervals. The present study was conducted to establish the extent of the deficit typical CI users have in understanding interrupted high-context sentences as a function of a range of interruption rates (1.5 to 24 Hz) and duty cycles (50 and 75 %). Further, factors such as reduced signal quality of CI signal transmission and advanced age, as well as potentially lower speech intelligibility of CI users even in the lack of interruption manipulation, were explored by presenting young, as well as age-matched, normal-hearing (NH) listeners with full-spectrum and vocoded speech (eight-channel and speech intelligibility baseline performance matched). While the actual CI users had more difficulties in understanding interrupted speech and taking advantage of faster interruption rates and increased duty cycle than the eight-channel noise-band vocoded listeners, their performance was similar to the matched noise-band vocoded listeners. These results suggest that while loss of spectro-temporal resolution indeed plays an important role in reduced intelligibility of interrupted speech, these factors alone cannot entirely explain the deficit. Other factors associated with real CIs, such as aging or failure in transmission of essential speech cues, seem to additionally contribute to poor intelligibility of interrupted speech.     

Solitary bone metastasis in the tibia as a presenting sign of endometrial adenocarcinoma: a case report and the review of the literature

Background Metastasis to bone from endometrial adenocarcinoma is rare, when metastasises it usually locates in axial skeleton. Metastasis to extremities is extremely rare. Additionally the detection of the bone metastasis as a presenting feature is uncommon. In the present study we report the 10th cases of bone metastasis in the literature which located at tibial diaphysis and originated from endometrial adenocarcinoma as a presenting feature of the primary disease. Case Single tibial lesion was observed in a 70 years old woman. Biopsy confirmed metastatic adenocarcinoma of the unknown origin. We couldn’t find the primary origin with aggressive work-up. Tibial lesion regressed with radiotherapy. Endometrial adenocarcinoma is detected after the end of disease-free one year with the symptom of vaginal bleeding. After 47 months from initial tibial lesion and 35 months from gynaecologic operation, patient is still alive and disease free. Discussion Patients with endometrial adenocarcinoma presenting an isolated skeletal metastasis may exhibit an unusual group with a better prognosis. This study was presented as a poster exhibition at the 5th Meeting of Asia-Pasific Musculo Skeletal Tumour Society held between 23 and 25, April 2004, Izmir, Turkey.     

Mast Cells Trigger Disturbed Bone Healing in Osteoporotic Mice

Mast cells are important tissue-resident sensor and effector immune cells but also play a major role in osteoporosis development. Mast cells are increased in numbers in the bone marrow of postmenopausal osteoporotic patients, and mast cell–deficient mice are protected from ovariectomy (OVX)-induced bone loss. In this study, we showed that mast cell–deficient Mcpt5-Cre R-DTA mice were protected from OVX-induced disturbed fracture healing, indicating a critical role for mast cells in the pathomechanisms of impaired bone repair under estrogen-deficient conditions. We revealed that mast cells trigger the fracture-induced inflammatory response by releasing inflammatory mediators, including interleukin-6, midkine (Mdk), and C-X-C motif chemokine ligand 10 (CXCL10), and promote neutrophil infiltration into the fracture site in OVX mice. Furthermore, mast cells were responsible for reduced osteoblast and increased osteoclast activities in OVX mice callus, as well as increased receptor activator of NF-κB ligand serum levels in OVX mice. Additional in vitro studies with human cells showed that mast cells stimulate osteoclastogenesis by releasing the osteoclastogenic mediators Mdk and CXCL10 in an estrogen-dependent manner, which was mediated via the estrogen receptor alpha on mast cells. In conclusion, mast cells negatively affect the healing of bone fractures under estrogen-deficient conditions. Hence, targeting mast cells might provide a therapeutic strategy to improve disturbed bone repair in postmenopausal osteoporosis. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).