Objective: Test D-methionine (D-met) as an otoprotectant from kanamycin-induced ototoxicity and determine the lowest maximally protective D-met dose. Design: Auditory brainstem responses (ABR) were measured at 4, 8, 14, and 20 kHz at baseline and two, four, and six weeks after kanamycin and D-met administration initiation. ABR threshold shifts assessed auditory function. Following six-week ABR testing, animals were decapitated and cochleae collected for outer hair cell (OHC) quantification. Study sample: Eight groups of 10 male pigmented guinea pigs were administered a subcutaneous kanamycin (250 mg/kg/dose) injection once per day and an intraperitoneal D-met injection (0 (saline), 120, 180, 240, 300, 360, 420, or 480 mg/kg/day) twice per day for 23 days. Results: Significant ABR threshold shift reductions and increased OHC counts (p 0.01) were measured at multiple D-met-dosed groups starting at two-week ABR assessments. A 300 mg/kg/day optimal otoprotective D-met dose provided 34-41 dB ABR threshold shift reductions and OHC protection. Lesser, but significant, D-met otoprotection was measured at lower and higher D-met doses. Conclusions: D-met significantly reduced ABR threshold shifts and increased OHC percentages compared to kanamycin-treated controls. Results may be clinically significant particularly for multidrug-resistant tuberculosis patients who frequently suffer from kanamycin-induced hearing loss in developing countries.

Peripheral gamma-delta T-cell proliferations are encountered in reaction to certain infections and in primary malignancies. Identifying sources of benign reactions is key in avoiding unnecessary workup and surveillance of these aggressive malignancies. Borrelia infections have been implicated in a number of lymphoproliferative disorders, but rarely, if ever, in this setting. While gamma-delta T-cells are known to play a prominent role in the immune response to Borrelia infection, B-cell differentiation is encountered in the majority of Borrelia-associated proliferations. We present here a unique case of benign-appearing peripheral gamma-delta T-cell lymphoid proliferation in the setting of a tick-bite with subsequent erythema migrans-like skin findings.

Sand boil formation due to underseepage is a potential failure mechanism for levees in the Lower Mississippi River Valley. Sand boils were identified in the Buck Chute study area in the 1990s during high-water events and during the 2009 Flood. The site is unique due to the presence of point bar and abandoned channel deposits. To understand the role of these alluvial deposits on sand boil formation at the site, a geologic investigation of the subsurface was conducted. Using shallow geophysics, cone penetrometer tests (CPT), borings, and a geographic information system (GIS), researchers concluded that the thin blanket associated with point bar deposits, abandoned channel deposits causing a blocked seepage path, and head differential changes caused by the Muddy Bayou Control Structure were the controls of sand boil formation at Buck Chute. DISCLAIMER: The contents of this report are not to be used for advertising, publication, or promotional purposes. Citation of trade names does not constitute an official endorsement or approval of the use of such commercial products. All product names and trademarks cited are the property of their respective owners. The findings of this report are not to be construed as an official Department of the Army position unless so designated by other authorized documents.

:Neurocristic hamartomas (NCH) of cutaneous origin are especially rare congenital or acquired neoplasms that often arise through aberrant embryologic development of pluripotent neural crest cells. Clinically, they often present as pigmented macules or papules on the scalp with associated alopecia. NCHs are characterized histopathologically by dermal melanocytic, fibroblastic, and neurosustentacular components. Correct identification of this etiology is critical because of potential for malignant transformation, particularly in acquired NCHs. Our patient was a 6-year-old girl with xeroderma pigmentosum and confirmed XPC mutation followed in our dermatology clinic since the age of 3. She had a history of multiple actinic keratoses but no prior skin cancers. A 4-mm homogenous pink papule on the left frontal scalp concerning for basal cell carcinoma was noted during routine skin examination. After a 3-month course of 3 times weekly topical imiquimod, the lesion had grown to a 6 mm diameter. The patient was then referred to plastic surgery for definitive excision. Histologically, the lesion showed a well-circumscribed proliferation of spindle cells with a trabecular and nested growth pattern. Perivascular pseudorosettes were identified, as were areas that resembled well-differentiated neural tissue. The spindle cells diffusely expressed S100 protein, SOX10, and CD34, with patchy expression of Melan-A and HMB-45. PRAME was negative, and p16 was retained. Array comparative genomic hybridization was performed, and no clinically significant copy number or single nucleotide variants were detected. To the best of our knowledge, this is the first documented case in the literature of a cutaneous neurocristic hamartoma arising in a patient with xeroderma pigmentosum.

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