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The characterization of diffusion through biological tissues has played an important role in fundamental medical research and product development. Understanding the diffusion phenomena allows for the identification of new concepts in fundamental science, evolving medical knowledge and improving future standards and protocols. To illustrate, the structure of cortical bone changes upon the onset of osteoporosis, altering the limited porous compartment through which nutrients and essential signaling molecules travel to bone cells. Estrogen hormone replacement therapy (HRT) is one of the gold standard treatments to attempt to mitigate the effects that this structural change exerts in menopausal osteoporosis patients; however, HRT effectiveness is often variable in these patients, likely due to variability in bone structure and physiology, and thus transport rates. Scientists have studied diffusion in cortical bone tissue for decades. Current methodological standards include fluorescence recovery after photobleaching and computed tomography finite element analysis. Both techniques limit areas of tissue to microscale (1-100 μm 2 ) analysis-only examining a few osteocytes within the structure at a time-and adopt assumptions that oversimplify in vivo tissue structure and transport phenomena. Also, the range of diffusion tracers is limited by the sensitivities of the analytical equipment, typically requiring tracer concentrations in the micromolar range. Herein is described a novel device for directly assessing the diffusion coefficient of 3 H-estradiol at 37°C in macroscale osteonal bone specimens (1.4 cm 2 )-assessing a much larger portion of the total tissue than previously reported-while using radioisotope tracers for much higher sensitivity, thus achieving physiologically relevant estradiol concentrations. The current diffusion chamber device represents a cost-effective and validated method to mitigate these shortcomings. The device provides long-term diffusion data through macroscale (greater than 1 mm 2 ) tissue areas, presenting a more physiologically accurate way to assess cortical bone diffusion. The device can assess solute diffusion through other tissues or materials and may easily be scaled up to run multiple diffusion experiments simultaneously. Impact statement The diffusion chamber device represents a cost-effective and validated method to assess solute diffusion through solid materials. Specifically, it demonstrates that this novel device provides long-term diffusion data through macroscale tissue samples at nanomolar concentrations, presenting a precise way to address the effects of tissue structures on diffusion. This device can be applied to other tissues or engineered materials, offering a methodology that is easily scaled up to allow simultaneous assessment of multiple material samples.

Identifying a complete, accurate model of brain function would allow neuroscientists and clinicians to make powerful neuropsychological predictions and diagnoses as well as develop more effective treatments to mitigate or reverse neuropathology. The productive model of brain function, which has been dominant in the field for centuries, cannot easily accommodate some higher-order neural processes associated with consciousness and other neuropsychological phenomena. However, in recent years, it has become increasingly evident that the brain is highly receptive to and readily emits electromagnetic (EM) fields and light. Indeed, brain tissues can generate endogenous, complex EM fields and ultraweak photon emissions (UPEs) within the visible and near-visible EM spectra. EM-based neural mechanisms, such as ephaptic coupling and non-visual optical brain signaling, expand canonical neural signaling modalities and are beginning to disrupt conventional models of brain function. Here, we present an evidence-based argument for the existence of brain processes that are caused by the transmission of extracerebral, EM signals and recommend experimental strategies with which to test the hypothesis. We argue for a synthesis of productive and transmissive models of brain function and discuss implications for the study of consciousness, brain health, and disease., Competing Interests: Conflicts of InterestThe authors report no conflict of interest, financial or otherwise., (© 2022 by the authors.)

Background: Posttraumatic stress disorder (PTSD) is associated with cognitive decline and risk for dementia, but the neuropathology involved is unclear., Objective: The aim of this study was to determine whether PTSD is associated with increased levels of Alzheimer's disease (AD) blood-based biomarkers., Methods: Individuals aged 50 years and older with PTSD were compared to trauma-exposed healthy controls (TEHCs) at baseline on serum measures of amyloid- β (A β ) 42 and 40 levels, the A β 42 /A β 40 ratio, and total tau. Serum was analyzed using ultrasensitive Simoa Human Neurology 3-Plex A assay (N3PA). Linear regressions modeling each AD biomarker as a function of group were used to investigate between-group differences, controlling for age, sex, and educational attainment (years)., Results: TEHC participants ( N  = 26) were 53.8% male with mean age 66.8±10.7, whereas PTSD participants ( N  = 44) were 47.7% male and aged 62.5±9.1 years. No between-group differences were noted on demographic characteristics or cognitive performance measured with the NIH Toolbox Cognition Battery. There were no significant between-group differences in serum A β 40 (TEHC 105.8±51.6 versus PTSD 93.2±56.1, p  = 0.46), A β 42 (TEHC 8.1±4.6 versus PTSD 7.8±4.6, p  = 0.63), A β 42 /A β 40 (TEHC 0.08±0.03 versus PTSD 0.09±0.03, p  = 0.27), or total tau (TEHC 0.5±0.3 versus PTSD 0.5±0.4, p  = 0.77). Likewise, there were no significant interaction effects of amyloid or tau serum concentrations and PTSD group status on cognitive functioning., Conclusion: Findings from cognitive assessments and serum analyses do not support PTSD-induced neurodegeneration of the Alzheimer's type as a pathway linking PTSD to increased incidence of dementia in older adults., Competing Interests: The authors have no conflicts of interest to report., (© 2022 – The authors. Published by IOS Press.)

Objective: Failure to diagnose and treat post-traumatic stress disorder (PTSD) may help explain the substantial disability, increased cognitive decline, and adverse health outcomes suffered by older adults with this disorder. To evaluate this possibility, we examined symptom differences among older and younger individuals with PTSD and measured the frequency with which older adults receive standard of care treatment., Methods: Clinician-Administered PTSD Scale for DSM (CAPS) scores were compared between younger and older adults with PTSD. Profiles were calculated for the most dominant CAPS symptom cluster reported by each participant, and the age cutoff best differentiating symptom clusters between individuals was determined. Clinical interview data (older adult sample only) were evaluated by trained raters to determine rates at which PTSD participants accessed treatment., Results: Among 108 individuals with PTSD, 69% of participants <67 years old had Criterion C (avoidance) symptoms as the most dominant cluster compared to 39% of participants ≥67 (p = 0.016). Eight percent of participants <67 years had Criterion E (hyperarousal) symptoms as the most dominant cluster compared to 30% of participants ≥67 (p = 0.016). Less than 25% of the older adults (N = 53 subsample) were receiving a first-line pharmacotherapy option for PTSD, and 0% of participants were currently participating in an evidence-based psychotherapy for PTSD., Conclusions: Clinicians evaluating patients should be aware that different symptom profiles may be present between younger and older adults with PTSD. Despite their high risk for adverse neuropsychiatric and other health consequences, older adults with PTSD appear to infrequently receive first-line clinical treatment., (© 2021 John Wiley & Sons Ltd.)

Selected polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) were detected by gas-chromatography coupled to triple quadrupole mass spectrometry (GC-QqQ-MS/MS) in marine sediments collected in central Italy. Total PCDD/Fs concentrations ranged from 11.58 to 193.29 pg/g d.w., with PCDFs as the major contributors in most cases. The congener profiles were characterized by high OCDD (70.7%-91.4%). The PCDD/Fs values are within or close to the Environmental Canada sediment reference values (0.85 pg TEQ/g d.w.). GC-QqQ-MS/MS can be a suitable alternative to standard methods for PCDD/Fs determination in environmental samples. The measured PCDD/Fs amounts could be considered as a basis for future monitoring programs.

Background and Aim of the Study: Recently published data suggest that prosthesis-patient mismatch is common after mitral valve replacement (MVR), and manifests as persistent pulmonary hypertension. The study aim was to determine the prevalence and severity of pulmonary hypertension after mitral valve surgery, including mitral valve repair, and to determine whether surgery type affects the prevalence of post-operative pulmonary hypertension., Methods: Matched preoperative and > or =1 year postoperative Doppler estimates of right ventricular systolic pressure (RVSP) were evaluated in a cohort of 179 patients who underwent MVR or repair (33 after bioprosthetic valve replacement, 20 after mechanical valve replacement, 43 after physiological valve repair (predominantly for myxomatous disease), 78 after undersized annuloplasty for functional regurgitation, and five after repair of rheumatic stenosis)., Results: Patients undergoing repair of function mitral regurgitation had a lower left ventricular ejection fraction. The postoperative mean transmitral gradient was slightly higher for patients after bioprosthetic valve replacement (6.9 +/- 2.6 mmHg) compared to mechanical valve replacement (5.2 +/- 2.8 mmHg; p = 0.03), physiological repair (5.2 +/- 2.8 mmHg; p = 0.05), or repair of functional regurgitation (5.5 +/- 2.8 mmHg; p = 0.02). Pulmonary hypertension was common (present in 78% of patients before and 64% after surgery), and there were no significant differences between groups in the prevalence of postoperative pulmonary hypertension. The RVSP tended to decrease in all groups, but reached statistical significance only for patients undergoing bioprosthetic replacement (-9 +/- 24 mmHg; p = 0.04), mechanical replacement (-10 +/- 14 mmHg; p = 0.003) or physiological repair (-6 +/- 16 mmHg; p = 0.01)., Conclusion: Pulmonary hypertension is common before and after mitral valve surgery. Although there were at least trends toward lower pulmonary artery pressures regardless of surgery type, significant decreases were noted only after MVR and physiological repair. A slightly higher postoperative mean transmitral gradient after bioprosthetic valve replacement may have contributed to postoperative pulmonary hypertension. The physiological repair of organic, non-rheumatic mitral regurgitation appears to offer favorable hemodynamics and a relatively low rate of postoperative pulmonary hypertension.