Dementia among Minority Populations: A Scoping Review of Meaning, Language, and Translation.

BACKGROUND: Dementia as a neurocognitive disorder is becoming increasingly common worldwide, and minority groups are more vulnerable than the general population. Many factors may contribute to their vulnerability such as misconceptions, language barriers, cultural factors, invalid assessment tools, lack of knowledge, or assigning spiritual beliefs to dementia symptoms. Therefore, this scoping literature review aimed to clarify how empirical studies reflect the meaning of dementia, language, and translation among minority ethnic groups. SUMMARY: The PRISMA extension for the scoping review protocol was used. Thirty-eight studies published in English were reviewed and analysed. The findings revealed that lack of knowledge about dementia and attributing the disease to the normal ageing process were frequent among minority groups. Furthermore, their cultural-specific perspectives and worldviews of wellness and well-being can impact the way dementia is perceived, consequent help-seeking behaviours, or caregiving. Facilitating educational programs to enhance the knowledge and experiences of ethnic communities might be beneficial. Moreover, language is shown to be an important aspect in dementia assessment and participants' educational level could significantly impact their functional capacity when responding to cognitive measures. Even though there are some useful screening tests, diagnosis barriers might be eased by assessment tool development, modifications, and accurate translations for ethnic communities. KEY MESSAGES: A promising pathway to support ethnically diverse communities regarding dementia can be raising awareness, providing ethnic-specific services, developing cultural-specific tools to assess dementia or any cognitive impairment by considering perceptions, language, and culture among ethnic groups. Cultural and spiritual considerations could also encourage engagement during assessment.

Initial Experience With Gallium-68 DOTA-Octreotate PET/CT and Peptide Receptor Radionuclide Therapy for Pediatric Patients With Refractory Metastatic Neuroblastoma.

RATIONALE: Pediatric patients with refractory neuroblastoma have limited therapeutic options. Neuroblastoma may express somatostatin receptors (SSTRs) allowing imaging with 68Ga-DOTA-Octreotate (GaTATE) positron emission tomography/computed tomography (PET/CT) and peptide receptor radionuclide therapy (PRRT). We reviewed our experience with this theranostic combination. MATERIALS AND METHODS: GaTATE studies (8 patients; 2 to 9 years old) were reviewed and compared with 123I-MIBG or posttreatment 131I-MIBG studies. Immunohistochemistry (IHC) for SSTR subtype 2 was performed in 5 patients. Four patients received PRRT. RESULTS: GaTATE PET showed additional disease in 38% (3/8 patients), and upstaged 1 patient by detecting marrow involvement. IHC detected SSTR 2 in all patients assessed. Six patients were deemed suitable for PRRT on imaging. Four patients received 17 cycles of palliative PRRT (10 111In-DOTATATE; 5 177Lu-DOTATATE; 1 combined 111In and 177Lu-DOTATATE; 1 combined 177Lu and 90Y-DOTATATE) with no significant toxicity attributed to PRRT. All had objective responses. Two survivors are now 40 and 56 months from PRRT commencement. CONCLUSIONS: GaTATE PET was positive in a high proportion of patients with refractory neuroblastoma, correlating with SSTR 2 on IHC, with additional disease identified compared with MIBG imaging. PRRT seems safe, feasible, with responses observed in patients with progression despite multimodality treatment. These data support ongoing clinical trials in such patients.

Diagnostic utility of p16INK4a: a reappraisal of its use in cervical biopsies.

p16(INK4a), an indirect marker of cell cycle dysregulation, is commonly expressed in cervical dysplasias and carcinomas associated with high risk human papillomavirus (HR-HPV) infections. Although p16(INK4a) immunohistology is routinely used as a cost effective surrogate marker, many of the published articles are confusing and contradictory. The discrepancies can be ascribed to a multitude of factors operating at the molecular, technical and interpretative levels. In the first place, our simplistic model of viral mediated oncogenesis is speculative and fails to account for all the known biomolecular changes. Unresolved technical issues include the variables of tissue fixation, antibody dilution, antibody isotype and clone, and the sensitivity of the particular detection method. Within any controlled staining method, strong diffuse or 'block' immunoreactivity in squamous cells may be found in moderate/severe dysplasia (CIN 2/3) and invasive squamous carcinoma. In contrast, focal or multifocal reactivity in squamous cells may be artefactual, related to low risk or HR-HPV. p16(INK4a) is less reliable when dealing with glandular lesions since considerable overlap exists between reactive and dysplastic lesions. In addition not all glandular dysplasias/carcinomas are HR-HPV related, nor are all p16(INK4a) immunoreactive lesions associated with HR-HPV. We conclude that p16(INK4a) immunoperoxidase shows greater specificity than sensitivity for squamous lesions; in comparison, glandular dysplasias/carcinomas show reduced specificity and sensitivity. Like all cell cycle regulatory proteins, the future diagnostic role of p16(INK4a) is limited. The ideal diagnostic molecular test for cervical dysplasias will detect a HR-HPV related product after, but not before, cell transformation and will reliably predict those cases yet to experience disease progression.