Patient navigation across the cancer care continuum: An overview of systematic reviews and emerging literature

Patient navigation is a strategy for overcoming barriers to reduce disparities and to improve access and outcomes. The aim of this umbrella review was to identify, critically appraise, synthesize, and present the best available evidence to inform policy and planning regarding patient navigation across the cancer continuum. Systematic reviews examining navigation in cancer care were identified in the Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, Embase, Cumulative Index of Nursing and Allied Health (CINAHL), Epistemonikos, and Prospective Register of Systematic Reviews (PROSPERO) databases and in the gray literature from January 1, 2012, to April 19, 2022. Data were screened, extracted, and appraised independently by two authors. The JBI Critical Appraisal Checklist for Systematic Review and Research Syntheses was used for quality appraisal. Emerging literature up to May 25, 2022, was also explored to capture primary research published beyond the coverage of included systematic reviews. Of the 2062 unique records identified, 61 systematic reviews were included. Fifty-four reviews were quantitative or mixed-methods reviews, reporting on the effectiveness of cancer patient navigation, including 12 reviews reporting costs or cost-effectiveness outcomes. Seven qualitative reviews explored navigation needs, barriers, and experiences. In addition, 53 primary studies published since 2021 were included. Patient navigation is effective in improving participation in cancer screening and reducing the time from screening to diagnosis and from diagnosis to treatment initiation. Emerging evidence suggests that patient navigation improves quality of life and patient satisfaction with care in the survivorship phase and reduces hospital readmission in the active treatment and survivorship care phases. Palliative care data were extremely limited. Economic evaluations from the United States suggest the potential cost-effectiveness of navigation in screening programs.     

Hippocampal damage and cytoskeletal disruption resulting from impaired energy metabolism

To determine if impaired energy metabolism might contribute to some aspects of Alzheimer disease (AD), including the vulnerability of the CA1 region of the hippocampal formation and the altered cytoskeleton evident in neurofibrillary tangles, we examined the effects of metabolic poisons on neuronal damage and cytoskeletal disruption in the hippocampal formation. Intrahippocampal injection of 3-nitropropionic acid (3-NP) and malonic acid resulted in neuronal death, particularly in CA1. Cytoskeletal disruption included loss of dendritic MAP2, but sparing of axonal τ. MK-801 (a noncompetitive NMDA receptor antagonist) did not atenuate the lesions produced by intrahippocampal injection of malonate. MK-801, however, was effective against intrastriatal malonate. Acute systemic 3-NP resulted in neuronal damage and cytoskeletal disruption in the CA1 region of the hippocampal formation, including an extensive loss of MAP2 immuno-reactivity, but sparing of τ. The neuronal loss in CA1 was delayed as compared to striatum. Chronic intraventricular infusion of 3-NP produced a different pattern of neuronal damage. Loss of τ-1 immuno-reactivity was observed in CA3 and CA1 s. oriens, whereas MAP2 immunostaining was preserved. These results demonstrate that chronic and acute administration of metabolic inhibitors produce distinct patterns of neuronal damage and cytoskeletal disruption. The results further suggest a differential involvement of the NMDA receptor in malonate-induced neuronal damage in striatum as compared to the hippocampus. The pattern of neuronal damage and cytoskeletal disruption observed following acute metabolic impairment resembled some aspects of neurofibrillary pathology in AD, but did not result in τ hyperphosphorylation.     

Digital radiography of the chest

Digital radiography is an appropriate method for both bedside and in-department chest radiographs. Its major advantage in bedside chest radiography is its control of the displayed optical density of these radiographs. With dynamic range control processing, it improves the visibility of tubes and lines superimposed on the mediastinal tissues. When used for in-department chest radiography, it may offer slight advantages in the evaluation of disease in the mediastinum, but in general is equivalent to film-screen chest radiography. The main reasons for using digital chest radiography for in-department chest radiographs relate mainly to its use as a data entry point method of projection radiography for high-quality teleradiology or for its use in a picture archiving and communication system. Apart from these advantages, there is no reason to change from conventional to digital chest radiographs. Digital radiographs are, with certain systems, printed at smaller than life size. Because of this, there is a necessary period of learning as radiologists adjust to the new image size. The most important change in radiologists' work pattern appears to be the need to sit closer to the film. Findings of disease are smaller, but, with experience, just as easy to see.     

Splenic injuries in children after blunt abdominal trauma

Management of splenic injuries in children has evolved over the past two decades. Splenectomies or splenorrhaphies are now performed infrequently, with the majority of hemodynamically stable children with splenic injuries managed nonoperatively. This article reviews the imaging features of acute splenic injuries in children as well as the appearance of healing splenic injuries. Follow-up evaluation and outcomes in children with splenic injuries also are addressed.     

Carbonate apatite crystals in primary normophosphatemic tumoral calcinosis

A 66‐year‐old woman developed firm, painless, slowly growing nodular masses over her elbows, fingers, toes, and left hip over four years. Aspiration of the elbow mass revealed a white chalky material that was shown to be carbonate apatite on infrared spectroscopy and energy dispersive X‐ray spectroscopy. We discuss the classification of tumoral calcinosis and the nature of the calcium deposits. Tumoral calcinosis should be differentiated from tophaceous gout and calcium pyrophosphate dihydrate crystal deposition disease. Polarizing light microscopy and crystal analysis by X‐ray and infrared spectroscopy, electron or X‐ray diffraction will confirm the diagnosis. Secondary causes of tumoral calcinosis should also be excluded.     

Issues and challenges in staging of pressure ulcers.

Wound assessment is a key element of effective wound care, and assessment of pressure ulcers includes accurate determination of wound stage. Although the original staging system established by Shea was based on his understanding of the pathology involved in pressure ulcer development, subsequent staging systems (and the one currently in use) were intended simply to establish the level of tissue damage. Recently, clinicians have drawn attention to numerous limitations associated with the current staging system, including the inability to differentiate between an inflammatory response involving intact skin and a deep tissue injury (deep bruising) underneath intact skin. This is a clinically significant difference because clinicians have noted that most inflammatory responses resolve with intervention, whereas most areas of deep tissue injury progress to full-thickness ulcers even when appropriate intervention is provided. A second area of controversy involves partial-thickness (Stage 2) lesions; because many of these lesions are caused by maceration and/or friction (as opposed to pressure) clinicians are frequently unclear regarding which of these lesions should be staged. In response to these concerns, the National Pressure Ulcer Advisory Panel convened a consensus forum and published white papers to clearly outline the issues; they solicited clinician feedback on the white papers and the Wound, Ostomy, Continence Nurses Society provided a written response. This article summarizes the key points of the white papers, WOCN Society response, and consensus forum discussion.     

Charge immobilization of the voltage sensor in domain IV is independent of sodium current inactivation

Recovery from fast inactivation in voltage-dependent Na⁺ channels is associated with a slow component in the time course of gating charge during repolarization (i.e. charge immobilization), which results from the slow movement of the S4 segments in domains III and IV (S4-DIII and S4-DIV). Previous studies have shown that the non-specific removal of fast inactivation by the proteolytic enzyme pronase eliminated charge immobilization, while the specific removal of fast inactivation (by intracellular MTSET modification of a cysteine substituted for the phenylalanine in the IFM motif, ICM_MTSET, in the inactivation particle formed by the linker between domains III and IV) only reduced the amount of charge immobilization by nearly one-half. To investigate the molecular origin of the remaining slow component of charge immobilization we studied the human cardiac Na⁺ channel (hH1a) in which the outermost arginine in the S4-DIV, which contributes ∼20% to total gating charge ( Q _max), was mutated to a cysteine (R1C-DIV). Gating charge could be fully restored in R1C-DIV by exposure to extracellular MTSEA, a positively charged methanethiosulphonate reagent. The RIC-DIV mutation was combined with ICM_MTSET to remove fast inactivation, and the gating currents of R1C-DIV-ICM_MTSET were recorded before and after modification with MTSEA_o. Prior to MTSEA_o, the time course of the gating charge during repolarization ( off -charge) was best described by a single fast time constant. After MTSEA, the off -charge had both fast and slow components, with the slow component accounting for nearly 35% of Q _max. These results demonstrate that the slow movement of the S4-DIV during repolarization is not dependent upon the normal binding of the inactivation particle.