Utilization of papanicolaou smears by South Asian women living in the United States

OBJECTIVES: Papanicolaou (Pap) smears are an underutilized screening modality among racial and ethnic minorities. However, no data exist on Pap smear utilization among South Asians, a rapidly growing population in the United States, whose country of origin includes India, Pakistan, Bangladesh, and Sri Lanka. We determined rates and identified variables associated with Pap smear receipt by South Asians. DESIGN: A self-administered survey instrument was mailed to a random sample of South Asians nationwide over a 3-month time period. South Asian households were identified by surnames that were used to search white pages in telephone directories, Department of Motor Vehicle records, and voter registries. Questions regarding Pap smear receipt were taken from the 1999 National Health Interview Survey. Sociodemographic information and measures of acculturation were obtained. PARTICIPANTS: A nationwide nonprobability sample of South Asian women. INTERVENTION: Cross-sectional observational study. MEASUREMENTS AND MAIN RESULTS: The overall response rate was 42%. In this sample, South Asians belonged to a high socioeconomic strata (SES), with 45% having a household income of >$80,000 and 42% having a master's degree. Three quarters of the respondents (73%) reported having a Pap smear in the last 3 years. In multivariate logistic regression analysis, South Asian women had greater odds of having had a Pap smear if they were married (P <.001), more educated (P =.004), had a usual source of care (P =.002), and were more acculturated (P =.004). CONCLUSIONS: Despite the high SES of South Asian women, their rates of Pap smear receipt were lower than national recommendations. Marital status, socioeconomic status, and acculturation are all associated with Pap smear receipt. South Asian communities should be targeted for outreach to promote Pap smear utilization.     

Natural products against cancer: Review on phytochemicals from marine sources in preventing cancer

Marine natural products have as of now been acknowledged as the most important source of bioactive substances and drug leads. Marine flora and fauna, such as algae, bacteria, sponges, fungi, seaweeds, corals, diatoms, ascidian etc. are important resources from oceans, accounting for more than 90% of the total oceanic biomass. They are taxonomically different with huge productive and are pharmacologically active novel chemical signatures and bid a tremendous opportunity for discovery of new anti-cancer molecules. The water bodies a rich source of potent molecules which improve existence suitability and serve as chemical shield against microbes and little or huge creatures. These molecules have exhibited a range of biological properties antioxidant, antibacterial, antitumour etc. In spite of huge resources enriched with exciting chemicals, the marine floras and faunas are largely unexplored for their anticancer properties. In recent past, numerous marine anticancer compounds have been isolated, characterized, identified and are under trials for human use. In this write up we have tried to compile about marine-derived compounds anticancer biological activities of diverse flora and fauna and their underlying mechanisms and the generous raise in these compounds examined for malignant growth treatment in the course of the most recent quite a long while.     

Towards enhanced community genetic literacy among a minority ethnic community: a participatory action research project

BackgroundInfant mortality is a key public health outcome showing substantial socioeconomic and ethnic inequalities in the UK. The UK Pakistani population has an infant mortality rate of over nine per 1000 livebirths, more than twice that for the population as a whole. Increased risk is partly attributable to rare autosomal recessive genetic disorders linked to the practice of customary consanguineous marriage. WHO recommends community-level action to raise genetic literacy combined with enhanced genetics services. However, UK interventions are in their infancy, with varied local initiatives and no national response. A combination of a valued social practice affecting marginalised communities, complicated patterns of risk, and low professional awareness, makes this a complex and contentious issue. Indeed, some previous intervention has generated considerable backlash. This study in Sheffield, a northern English city, aimed to develop a community-level genetic literacy intervention that would be sensitive and responsive to local information needs.MethodsA participatory approach was used, drawing on a user-centred design and engaging local people as coresearchers. Two phases of insight gathering made use of group discussions, interviews, and participatory exercises to describe current understanding, gaps in knowledge, and trusted networks of communication. A series of testing-and-refinement cycles were then undertaken to coproduce a set of communication materials tailored to subgroups, with materials being tested for acceptability, appeal, and comprehension.FindingsSix local people were trained as coresearchers. Over 200 people participated in the insight and testing work. Information needs and preferred communication channels varied widely, confirming population heterogeneity and diverse perspectives to the issue. Despite some resistance, there was strong demand for information and willingness to discuss the topic. Conveying accurate and consistent information was challenging, as was meeting differing demands for detail within generic materials. Key areas of confusion and mistrust were addressed. Narrative, real life audio (for local radio) and video (for social media) were recommended and developed, supported by factual information in leaflet and website form, and contained links to religious resources plus genetics services.InterpretationDevelopment of appropriate community-level genetic literacy interventions can be achieved through participatory action research. Evaluative work is now needed to assess the effect on knowledge and service uptake.FundingGenetics Disorders UK funded the study. SS is a Senior Research Fellow funded by the National Institute for Health Research (NIHR) School for Public Health Research. Preparatory work was funded by NIHR Collaboration for Leadership in Applied Health Research & Care for South Yorkshire.     

Interneuron precursor transplants in adult hippocampus reverse psychosis-relevant features in a mouse model of hippocampal disinhibition

GABAergic interneuron hypofunction is hypothesized to underlie hippocampal dysfunction in schizophrenia. Here, we use the cyclin D2 knockout (Ccnd2^−/−) mouse model to test potential links between hippocampal interneuron deficits and psychosis-relevant neurobehavioral phenotypes. Ccnd2^−/− mice show cortical PV⁺ interneuron reductions, prominently in hippocampus, associated with deficits in synaptic inhibition, increased in vivo spike activity of projection neurons, and increased in vivo basal metabolic activity (assessed with fMRI) in hippocampus. Ccnd2^−/− mice show several neurophysiological and behavioral phenotypes that would be predicted to be produced by hippocampal disinhibition, including increased ventral tegmental area dopamine neuron population activity, behavioral hyperresponsiveness to amphetamine, and impairments in hippocampus-dependent cognition. Remarkably, transplantation of cells from the embryonic medial ganglionic eminence (the major origin of cerebral cortical interneurons) into the adult Ccnd2^−/− caudoventral hippocampus reverses these psychosis-relevant phenotypes. Surviving neurons from these transplants are 97% GABAergic and widely distributed within the hippocampus. Up to 6 mo after the transplants, in vivo hippocampal metabolic activity is lowered, context-dependent learning and memory is improved, and dopamine neuron activity and the behavioral response to amphetamine are normalized. These findings establish functional links between hippocampal GABA interneuron deficits and psychosis-relevant dopaminergic and cognitive phenotypes, and support a rationale for targeting limbic cortical interneuron function in the prevention and treatment of schizophrenia.Precursors of most γ-aminobutyric acid (GABA)-releasing interneurons of the cerebral cortex and the hippocampus originate in the embryonic medial ganglionic eminence (MGE) (1–3). A subpopulation of MGE-derived cells differentiates into fast-spiking, parvalbumin-expressing (PV⁺) interneurons that tightly regulate the activity and synchronization of cortical projection neurons (2, 4). Structural and functional deficits in PV⁺ interneurons are hypothesized as a pathophysiological mechanism in schizophrenia and psychotic disorders (4–6).Although psychotic disorders are clearly heterogeneous in etiology, disinhibition within temporolimbic cortical circuits is postulated as a core pathophysiology underlying positive symptoms (e.g., delusions and hallucinations) and a subset of cognitive disturbances that manifest with psychosis (4, 5, 7). Postmortem studies of brains from individuals with psychotic disorders show reduced molecular markers of the number and/or function of PV⁺ interneurons in the hippocampus (6, 8). Consistent with these observations, basal metabolic activity in the hippocampus, as measured with functional magnetic resonance imaging (fMRI), is increased in schizophrenia, a phenotype that predicts psychosis and positive symptom severity (5, 7). This abnormal resting activity is postulated to underlie abnormal recruitment of hippocampal circuits during cognitive performance (5, 9). Striatal dopamine (DA) release capacity is also increased and correlated with positive symptoms in schizophrenia and its risk states (10, 11). Importantly, hippocampal hyperactivity may contribute to DA dysregulation (12), because rodent studies show that caudoventral hippocampal (in the primate, anterior hippocampal) efferents regulate the activity of DA neurons and medial striatal DA release (13, 14).Thus, converging evidence implicates hippocampal disinhibition in the abnormal striatal DA transmission and cognitive impairment in schizophrenia. However, the role of hippocampal inhibitory interneurons in psychosis-relevant circuitry remains to be established. To this end, we used the cyclin D2 (Ccnd2) knockout mouse model (15), which displays a relatively selective deficit in cortical PV⁺ interneurons, and transplantation of interneuron precursors from the MGE to elucidate relationships between reduced hippocampal GABA interneuron function and multiple psychosis-relevant phenotypes, and to explore a novel treatment strategy for psychosis.     

Improved quantification of amyloid burden and associated biomarker cut-off points: results from the first amyloid Singaporean cohort with overlapping cerebrovascular disease

European Journal of Nuclear Medicine and Molecular Imaging - The analysis of the [11C]PiB-PET amyloid images of a unique Asian cohort of 186 participants featuring overlapping vascular diseases...     

Correction: Acridinedione as selective flouride ion chemosensor: a detailed spectroscopic and quantum mechanical investigation

Correction for ‘Acridinedione as selective flouride ion chemosensor: a detailed spectroscopic and quantum mechanical investigation’ by Nafees Iqbal et al., RSC Adv., 2018, 8, 1993–2003.

The authors regret that the interpretation of the fluorescence spectra of compound 7i published in the original article was incorrect. In the original article, it was reported that upon excitation at 380 nm, the fluorescence spectrum of compound 7i showed two emission bands at 450 nm and 770 nm (Fig. 5b of the original article). The signal at 770 nm (previously reported as an emission band), is instead a second order diffraction (an artefact of diffraction grating/spectrofluorometer monochromator), as revealed from the literature.^1,2 The authors thank a reader for highlighting this mistake.The Royal Society of Chemistry apologises for these errors and any consequent inconvenience to authors and readers.     

Urotensin I-like immunoreactivity in amacrine cells of the goldfish retina

Urotensin I-like immunoreactivity (UILI), in different localization from that of corticotropin releasing factor-like immunoreactivity (CRFLI), in the goldfish retina has been demonstrated by means of radioimmunoassay, high-performance liquid chromatography (HPLC) and immunohistochemistry. Radioimmunoassay showed 350 +/- 40 pg/mg prot. of UILI in goldfish retina extracts. The immunoreactive material present in the retina was also characterized by reversed phase HPLC. Some of the UILI co-eluted with synthetic carp UI, though the HPLC experiments suggested the existence of other UILI substance(s) with less hydrophobicity than synthetic UI. By immunohistochemistry, UILI and CRFLI were seen in different amacrine cells of the goldfish retina. It is suggested that UI may be involved in the fish visual transmission system together with CRF and other neuropeptides.     

A systematic review of the relationship between glycemic control and necrobiosis lipoidica diabeticorum in patients with diabetes mellitus

The association of specific skin disorders with diabetes mellitus (DM) has been well established. Current literature suggests that approximately 30–91% of patients with diabetes will experience at least one cutaneous manifestation of this systemic disease in their lifetime. To date, there are limited articles summarizing the link between necrobiosis lipoidica diabeticorum (NLD) prognosis and glycemic control in patients with diabetes. The objective of the study is to summarize and appraise the available evidence assessing the relationship between glycemic control and NLD. A literature search was conducted based on MEDLINE (1946–2015), EMBASE (1980–2015), Google Scholar, and PubMed for publications that described the results of diabetes control and NLD. Further studies were identified from bibliographies of all relevant studies, gray literature, and annual scientific assemblies. All studies investigating the relationship between DM (type 1 and type 2) management and NLD were included. Two reviewers independently extracted data including demographics, type of diabetes management measures (glucose, HbA1c, insulin), comorbidities, and outcome. A total of 622 studies were identified, and 10 studies met the inclusion and exclusion criteria: two case series and eight case reports. Of the 24 patients with NLD, 13 patients reported resolution of NLD after implementing various methods of glycemic control (diabetic diet consisting of 1600 kcal/day [1 patient], insulin regimen [3 patients], and pancreatic transplantation [9 patients]). Glycemic control may have a role in influencing the prognosis of necrobiosis lipoidica in patients with diabetes; however, there is currently insufficient evidence to support or refute this claim.     

Enhancement of dentate gyrus neurogenesis, dendritic and synaptic plasticity and memory by a neurotrophic peptide

Pharmacological enhancement of hippocampal neurogenesis is a therapeutic approach for improvement of cognition in learning and memory disorders such as Alzheimer's disease. Here we report the development of an 11-mer peptide that we designed based on a biologically active region of the ciliary neurotrophic factor. This peptide, Peptide 6, induced proliferation and increased survival and maturation of neural progenitor cells into neurons in the dentate gyrus of normal adult C57BL6 mice. Furthermore, Peptide 6 increased the MAP2 and synaptophysin immunoreactivity in the dentate gyrus. Thirty-day treatment of the mice with a slow release bolus of the peptide implanted subcutaneously improved reference memory of the mice in Morris water maze. Peptide 6 has a plasma half life of over 6 h, is blood-brain barrier permeable, and acts by competitively inhibiting the leukemia inhibitory factor signaling. The fact that Peptide 6 is both neurogenic and neurotrophic and that this peptide is effective when given peripherally, demonstrates its potential for prevention and treatment of learning and memory disorders.     

HIF inhibitors for ischemic retinopathies and cancers: options beyond anti-VEGF therapies

Aberrant activation of the hypoxia inducible factor (HIF) pathway causing overexpression of angiogenic genes, like vascular endothelial growth factor (VEGF), is one of the underlying causes of ocular neovascularization (NV) and metastatic cancer. Consistently, along with surgical interventions, a number of anti-VEGF agents have been approved by FDA for the treatment of ocular neovascular diseases. These anti-VEGF agents, like ranibizumab/lucentis, have revolutionized the treatment in the past decade. However, substantial vision improvement is observed only in a subset of age-related macular degeneration patients receiving ranibizumab. Further, all current therapies are associated with limitations and side effects. For example, surgeries cause tissue destruction and inflammation while anti-VEGF therapies are expensive, require repeated administration, and offer temporary relief from vascular leakage. These factors impose significant cost and treatment burdens to both the patient and society. With an aging population in most western countries with a continually increasing number of patients on lifelong treatment for these retinal diseases, the focus of ocular drug development for neovascular diseases will be to improve efficacy while reducing treatment costs. Blocking the HIF pathway, a major regulator of ocular NV and cancer, offers an appealing therapeutic strategy. Therefore, this review summarizes HIF inhibitors that have been recently evaluated for the treatment of different cancers and ischemic retinopathies.