Human-machine interface (HMI) designs offer the possibility of improving quality of life for patient populations as well as augmenting normal user function. Despite pragmatic benefits, utilizing auditory feedback for HMI control remains underutilized, in part due to observed limitations in effectiveness. The goal of this study was to determine the extent to which categorical speech perception could be used to improve an auditory HMI. Using surface electromyography, 24 healthy speakers of American English participated in 4 sessions to learn to control an HMI using auditory feedback (provided via vowel synthesis). Participants trained on 3 targets in sessions 1–3 and were tested on 3 novel targets in session 4. An “established categories with text cues” group of eight participants were trained and tested on auditory targets corresponding to standard American English vowels using auditory and text target cues. An “established categories without text cues” group of eight participants were trained and tested on the same targets using only auditory cuing of target vowel identity. A “new categories” group of eight participants were trained and tested on targets that corresponded to vowel-like sounds not part of American English. Analyses of user performance revealed significant effects of session and group (established categories groups and the new categories group), and a trend for an interaction between session and group. Results suggest that auditory feedback can be effectively used for HMI operation when paired with established categorical (native vowel) targets with an unambiguous cue.
Wilson's disease (WD) is a rare liver disease characterized by copper accumulation. Interestingly, iron overload has been observed in patients with WD without a diagnosis of primary hemochromatosis. This association has been recognized in the literature for almost two decades. 1-3 Of the chronic liver diseases known to cause secondary hemochromatosis, WD is classically not listed among them. The prevalence of secondary hemochromatosis in patients with WD is unknown. Despite the rarity of this disease, this knowledge is important because it yields therapeutic and monitoring implications in patients with WD. This article will begin with a review of the etiology and pathophysiology of WD, as well as the iron overload syndromes, followed by an explanation of the mechanism of secondary hemochromatosis in patients with WD. Finally, the authors will discuss the clinical implications of this knowledge with a focus on therapeutics. HePaTiC MeTal sTOraGe DisOrDers: COPPer anD irOn The mechanisms of hepatic transport of copper and iron are intimately related. 1 This relatedness can be observed in pathological states. 1 WD is a disorder of copper metabolism that is caused by mutations in the ATP7B gene, which codes for a copper transport protein in the liver. 4-6 The absent or compromised ATP7B protein not only causes copper accumulation in the liver and other organs but also reduces the amount of circulating ceruloplasmin. 4-6 Normally, the ATP7B protein loads copper onto ceruloplasmin, the primary means of copper transport throughout the body (Fig. 1). 1,7 In WD, the inability of the ATP7B protein to transport copper and thus facilitate its secretion through the biliary system leads to copper accumulation in the liver. 8,9 Copper accumulation and toxicity lead to hepatic, neurological, and psychiatric dysfunction, and
Objective: Acquired reactive perforating collagenosis is an uncommon skin disease that belongs to a group of dermatologic disorders characterized by transepidermal elimination of dermal material. It is highly associated with systemic disease, primarily diabetes mellitus and dialysisdependent chronic renal failure. Methods: A 70-year-old female with 20 years of poorly controlled type 2 diabetes mellitus presented with a 6-month history of multiple pruritic erythematous papules and nodules with central hyperkeratosis, involving her right dorsal arm. Histologic examination was consistent with acquired reactive perforating collagenosis. In addition to topical treatment of the disease, the patient was referred to endocrinology for appropriate management of her underlying diabetes mellitus. Results: Ideal treatment should involve both the endocrinologist and dermatologist. Control of the underlying systemic disease, in this case diabetes, as well topical or systemic medications can both help to improve this condition. Our patient re-established care with her endocrinologist who adjusted her medication regimen, resulting in improved hemoglobin A1c values. Our patient additionally benefited from topical betamethasone cream, ammonium lactate, and pimecrolimus application. The combined therapy led to resolution of her pruritic rash. Conclusion: This case highlights the importance of the skin exam by the endocrinologist, as he or she plays a unique role in identifying this rare and difficult-to-treat dermatologic disease. Early detection and prompt referral to a dermatologist are crucial in preventing progression of disease, treating the disease, and improving the patient's quality of life. (AACE Clinical Case Rep.
Casestudy: The utilization of checkpoint inhibitors such as programmed cell death protein 1 (PD-1/PD-L1) inhibitors (nivolumab) and cytotoxic T-lymphocyte antigen 4 inhibitors (ipilimumab) for treatment of certain malignancies has steadily gained popularity. Medication related colitis is uncommon, with a reported incidence of 1–9% depending on the checkpoint inhibitor used, and the histologic features have been characterized in recent literature. Because of the immunomodulating effect of these drugs, infectious colitis is in the differential diagnosis of enteritis. Multi-drug therapy in many of these patients further complicates identification of the culprit drug. We present the case of a 63-year-old male with metastatic renal cell carcinoma being treated with both nivolumab and ipilimumab who presented with acute on chronic non-bloody diarrhea. His clinical course was complicated by hypotension, acidosis and coagulopathy. The clinical differential for his colitis was cytomegalovirus infection versus a checkpoint inhibitor colitis. Colonoscopy revealed continuous circumferential loss of vascularity and diffuse erythema throughout the colon. Histology showed acute colitis with prominent apoptosis, cryptitis, crypt abscesses, and rare ringed mitotic figures, but without architectural distortion. Occasional smooth purple crystals consistent with pill material were present in the mucosa, but without significant tissue reaction. No pathogenic organisms were identified, and a cytomegalovirus immunostain was negative. These histologic findings in concert with the clinical history are consistent with checkpoint inhibitor colitis and multi-drug effect. A review of the patient’s chart showed cholestyramine was added to the patient’s regimen during hospitalization, which was consistent with the morphologic appearance of the crystals. Given the acute complications of checkpoint inhibitor induced enterocolitis and potential for increased morbidity (rare cases of bowel perforation and subsequent resection), accurate diagnosis is imperative. Management of checkpoint inhibitor associated colitis ranges from initiation of immunosuppression to checkpoint inhibitor cessation. When these findings are masked by multi-drug effect, accurate diagnosis can be difficult.
We present a case of an 85-year-old female who received a bone marrow biopsy for concern over myelodysplastic symptoms and was subsequently diagnosed with a CD138-positive metastatic lobular breast carcinoma that mimicked a plasma cell neoplasm. Her medical history included endometrial serous adenocarcinoma (pT1a N0), severe mitral regurgitation, and atrial fibrillation. She presented with a 3-month history of thrombocytopenia (60,000/mcL) and a down-trending macrocytic anemia (nidus hemoglobin: 6-7 g/dL) that prompted a bone marrow biopsy. The aspirate smears were aparticulate and hemodiluted, while the touch preparations revealed a homogeneous population of large, plasmacytoid cells. These were again seen filling the medullary cavity on the bone marrow biopsy with eccentrically placed nuclei containing nucleoli and abundant eosinophilic cytoplasm. The cells were CD138, cytokeratin 7 and 8/18, mammoglobulin, and GATA-3 positive. They were cytokeratin 20, TTF-1/Napsin, PAX-8, and uroplakin negative. Further testing revealed the cells to be estrogen receptor positive (strong, 90%+), progesterone negative, HER2 negative, p120 positive (strong cytoplasmic), and E-cadherin negative. The patient’s prior serous adenocarcinoma histomorphology was not consistent with the plasmacytoid cells. Prior literature revealed a case report on a metastatic lobular carcinoma to bone marrow and discussion on the morphologic similarities, but the case was CD138 negative. This case highlights that CD138 can be positive in certain carcinomas, some of which can have a plasmacytoid morphology. Suspicion should be raised in an elderly female population.
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