A pilot survey of students' menstrual attitudes, experiences, and needs on an urban university campus.

BACKGROUND: In the United States, many menstruators face barriers to period management, such as period poverty, or the lack of access to relevant knowledge and affordable menstrual products. Our current understanding of the social, emotional, and physical impacts of period poverty on students in post-secondary institutions is largely limited. OBJECTIVES: The purpose of this pilot study is to assess period poverty, period-related class disruption, and avoidance of menstrual hygiene management on campus among students and to identify recommendations for action at the University of Illinois Chicago and other urban universities. DESIGN: An online cross-sectional study from February to May 2023. METHODS: Enrolled students who were at least 18 years old completed an anonymous, self-administered online survey. Through descriptive statistics and chi-square tests in SAS version 9.4, we analyzed the sociodemographic, academic, and menstrual characteristics of those who had a period in the past 12 months. We also performed a thematic analysis of students' open-ended responses regarding their menstrual experiences on campus. RESULTS: Of our sample (N = 106), 17.1% of students have faced period poverty, 55.8% experienced period-related class disruption, and 47.5% avoided changing their menstrual products on campus. The relationships between the three menstrual experiences were statistically significant. In the open responses, students reported that their personal experiences with menstruation were largely painful and disruptive. We identified the following themes: (1) inadequate water, sanitation, and hygiene facilities; (2) understocked, empty, or non-existent menstrual product dispensers; (3) a desire for additional resources for menstruation; and (4) the unpredictability of menstruation. CONCLUSION: Our findings indicate that students continue to face obstacles to menstruation management due to inadequate support related to menstrual infrastructure, products, and pain. We outline several recommendations for university/college institutions to prioritize a more inclusive and supportive educational environment for all students.

Students' experiences of menstrual periods while on an urban university campusIn the United States, many girls, women, and other menstruators encounter challenges while managing their menstrual periods. Such barriers include period poverty, or the inability to afford resources and menstrual products such as tampons or pads. In this study, we explored how period poverty impacts college/university students. We shared an online survey with 106 students who were older than 18 years, had a period in the last 12 months, and attended the University of Illinois Chicago. We asked them about their menstrual, social, and academic experiences. We found that approximately one in six students could not afford menstrual products at some point in their lives, over half missed all or portions of class due to their period, and about one in two students avoided changing their menstrual products on campus. The relationships between these three menstrual experiences were statistically significant. Many students also reported that periods were largely painful, disruptive, and unpredictable and that their campus had few physical resources and more obstacles to managing menstruation. From our findings, we identified several steps that universities and colleges can take to prioritize a more inclusive and supportive educational environment for all students.

The neuropathological landscape of small vessel disease and Lewy pathology in a cohort of Hispanic and non-Hispanic White decedents with Alzheimer disease.

Cerebrovascular and α-synuclein pathologies are frequently observed alongside Alzheimer disease (AD). The heterogeneity of AD necessitates comprehensive approaches to postmortem studies, including the representation of historically underrepresented ethnic groups. In this cohort study, we evaluated small vessel disease pathologies and α-synuclein deposits among Hispanic decedents (HD, n = 92) and non-Hispanic White decedents (NHWD, n = 184) from three Alzheimer's Disease Research Centers: Columbia University, University of California San Diego, and University of California Davis. The study included cases with a pathological diagnosis of Intermediate/High AD based on the National Institute on Aging- Alzheimer's Association (NIA-AA) and/or NIA-Reagan criteria. A 2:1 random comparison sample of NHWD was frequency-balanced and matched with HD by age and sex. An expert blinded to demographics and center origin evaluated arteriolosclerosis, cerebral amyloid angiopathy (CAA), and Lewy bodies/Lewy neurites (LBs/LNs) with a semi-quantitative approach using established criteria. There were many similarities and a few differences among groups. HD showed more severe Vonsattel grading of CAA in the cerebellum (p = 0.04), higher CAA density in the posterior hippocampus and cerebellum (ps = 0.01), and increased LBs/LNs density in the frontal (p = 0.01) and temporal cortices (p = 0.03), as determined by Wilcoxon's test. Ordinal logistic regression adjusting for age, sex, and center confirmed these findings except for LBs/LNs in the temporal cortex. Results indicate HD with AD exhibit greater CAA and α-synuclein burdens in select neuroanatomic regions when compared to age- and sex-matched NHWD with AD. These findings aid in the generalizability of concurrent arteriolosclerosis, CAA, and LBs/LNs topography and severity within the setting of pathologically confirmed AD, particularly in persons of Hispanic descent, showing many similarities and a few differences to those of NHW descent and providing insights into precision medicine approaches.

Improvement in Cardiac Morphology Demonstrated by Cardiac Magnetic Resonance Imaging and Echocardiography after Haploidentical Hematopoietic Cell Transplantation in Adults with Sickle Cell Disease.

Cardiopulmonary complications account for approximately 40% of deaths in patients with sickle cell disease (SCD). Diffuse myocardial fibrosis, elevated tricuspid regurgitant jet velocity (TRV) and iron overload are all associated with early mortality. Although HLA-matched sibling hematopoietic cell transplantation (HCT) offers a potential cure, less than 20% of patients have a suitable donor. Haploidentical HCT allows for an increased donor pool and has recently demonstrated improved safety and efficacy. Our group has reported improved cardiac morphology via echocardiography at 1 year after HCT. Here we describe the first use of cardiac magnetic resonance imaging (CMR), the gold standard for measuring volume, mass, and ventricular function, to evaluate changes in cardiac morphology post-HCT in adults with SCD. We analyzed baseline and 1-year data from 12 adults with SCD who underwent nonmyeloablative haploidentical peripheral blood HCT at the National Institutes of Health. Patients underwent noncontrast CMR at 3 T, echocardiography, and laboratory studies. At 1 year after HCT, patients showed marked improvement in cardiac chamber morphology by CMR, including left ventricular (LV) mass (70.2 to 60.1 g/m2; P = .02) and volume (114.5 to 90.6 mL/m2; P = .001). Furthermore, mean TRV normalized by 1 year, suggesting that HCT may offer a survival benefit. Fewer patients had pathologically prolonged native myocardial T1 times, an indirect marker of myocardial fibrosis at 1 year; these data showed a trend toward significance. In this small sample, CMR was very sensitive in detecting cardiac mass and volume changes after HCT and provided complementary information to echocardiography. Notably, post-HCT improvement in cardiac parameters can be attributed only in part to the resolution of anemia; further studies are needed to determine the roles of myocardial fibrosis reversal, improved blood flow, and survival impact after HCT for SCD.

The neuropathological landscape of Hispanic and non-Hispanic White decedents with Alzheimer disease.

Despite the increasing demographic diversity of the United States' aging population, there remain significant gaps in post-mortem research investigating the ethnoracial heterogeneity in the neuropathological landscape of Alzheimer Disease (AD). Most autopsy-based studies have focused on cohorts of non-Hispanic White decedents (NHWD), with few studies including Hispanic decedents (HD). We aimed to characterize the neuropathologic landscape of AD in NHWD (n = 185) and HD (n = 92) evaluated in research programs across three institutions: University of California San Diego, University of California Davis, and Columbia University. Only persons with a neuropathologic diagnosis of intermediate/high AD determined by NIA Reagan and/or NIA-AA criteria were included. A frequency-balanced random sample without replacement was drawn from the NHWD group using a 2:1 age and sex matching scheme with HD. Four brain areas were evaluated: posterior hippocampus, frontal, temporal, and parietal cortices. Sections were stained with antibodies against Aß (4G8) and phosphorylated tau (AT8). We compared the distribution and semi-quantitative densities for neurofibrillary tangles (NFTs), neuropil threads, core, diffuse, and neuritic plaques. All evaluations were conducted by an expert blinded to demographics and group status. Wilcoxon's two-sample test revealed higher levels of neuritic plaques in the frontal cortex (p = 0.02) and neuropil threads (p = 0.02) in HD, and higher levels of cored plaques in the temporal cortex in NHWD (p = 0.02). Results from ordinal logistic regression controlling for age, sex, and site of origin were similar. In other evaluated brain regions, semi-quantitative scores of plaques, tangles, and threads did not differ statistically between groups. Our results demonstrate HD may be disproportionately burdened by AD-related pathologies in select anatomic regions, particularly tau deposits. Further research is warranted to understand the contributions of demographic, genetic, and environmental factors to heterogeneous pathological presentations.

TDP-43 Pathology in the Setting of Intermediate and High Alzheimer's Disease Neuropathologic Changes: A Preliminary Evaluation Across Ethnoracial Groups.

BACKGROUND: Transactive Response DNA Binding Protein 43 kDa (TDP-43) pathology is frequently found in cases with Alzheimer's disease (AD). TDP-43 pathology is associated with hippocampal atrophy and greater AD severity denoted by cognition and clinical representation. Current TDP-43 pathology studies are predominantly based on non-Hispanic White cohorts. OBJECTIVE: We sought to evaluate the presence of TDP-43 pathology across ethnoracial groups utilizing the National Alzheimer's Coordinating Center; a database containing data from over 29 institutions across the United States. Cases (N = 1135: Hispanics/Latinos = 29, African Americans/Black Americans = 51, Asians/Asian Americans = 10, American Indians/Alaskan Natives = 2, non-Hispanic White = 1043) with intermediate/high AD having data on TDP-43 pathology in the amygdala, hippocampus, entorhinal cortex, and neocortex were included. METHODS: TDP-43 pathology frequency in each neuroanatomic region among ethnoracial groups were compared using generalized linear mixed effects models with center as a random effect adjusting for age at death, education, and gender. RESULTS: Although groups were imbalanced, there was no significant difference across ethnoracial groups based on TDP-43 pathology (p = 0.84). With respect to neuroanatomical regions evaluated, there were no significant differences across ethnoracial groups (p-values > 0.06). There were also no significant differences for age at death and gender ratios across ethnoracial groups based on TDP-43 pathology. Although not statistically significant, TDP-43 pathology was present less often in Hispanic/Latinos (34%) when compared to non-Hispanic Whites (46%). CONCLUSION: While this is a preliminary evaluation, it highlights the need for diverse cohorts and on TDP-43 pathology research across ethnoracial groups. This is the first study to our knowledge having a focus on the neuroanatomical distribution of TDP-43 deposits in Hispanic/Latino decedents with AD.

Elastin Insufficiency Confers Proximal and Distal Pulmonary Vasculopathy in Mice, Partially Remedied by the KATP Channel Opener Minoxidil: Considerations and Cautions for the Treatment of People With Williams-Beuren Syndrome.

Background: Williams Beuren syndrome (WBS) is a recurrent microdeletion disorder that removes one copy of elastin (ELN), resulting in large artery vasculopathy. Early stenosis of the pulmonary vascular tree is common, but few data are available on longer-term implications of the condition. Methods: Computed tomography (CT) angiogram (n = 11) and echocardiogram (n = 20) were performed in children with WBS aged 3.4-17.8 years. Controls (n = 11, aged 4.4-16.8 years) also underwent echocardiogram. Eln +/- mice were analyzed by invasive catheter, echocardiogram, micro-CT (µCT), histology, and pressure myography. We subsequently tested whether minoxidil resulted in improved pulmonary vascular endpoints. Results: WBS participants with a history of main or branch pulmonary artery (PA) stenosis requiring intervention continued to exhibit increased right ventricular systolic pressure (RVSP, echocardiogram) relative to their peers without intervention (p < 0.01), with no clear difference in PA size. Untreated Eln +/- mice also show elevated RVSP by invasive catheterization (p < 0.0001), increased normalized right heart mass (p < 0.01) and reduced caliber branch PAs by pressure myography (p < 0.0001). Eln +/- main PA medias are thickened histologically relative to Eln +/+ (p < 0.0001). Most Eln +/- phenotypes are shared by both sexes, but PA medial thickness is substantially greater in Eln +/- males (p < 0.001). Eln +/- mice showed more acute proximal branching angles (p < 0.0001) and longer vascular segment lengths (p < 0.0001) (µCT), with genotype differences emerging by P7. Diminished PA acceleration time (p < 0.001) and systolic notching (p < 0.0001) were also observed in Eln +/- echocardiography. Vascular casting plus µCT revealed longer generation-specific PA arcade length (p < 0.0001), with increased PA branching detectable by P90 (p < 0.0001). Post-weaning minoxidil decreased RVSP (p < 0.01) and normalized PA caliber (p < 0.0001) but not early-onset proximal branching angle or segment length, nor later-developing peripheral branch number. Conclusions: Vascular deficiencies beyond arterial caliber persist in individuals with WBS who have undergone PA stenosis intervention. Evaluation of Eln +/- mice reveals complex vascular changes that affect the proximal and distal vasculatures. Minoxidil, given post-weaning, decreases RVSP and improves lumen diameter, but does not alter other earlier-onset vascular patterns. Our data suggest additional therapies including minoxidil could be a useful adjunct to surgical therapy, and future trials should be considered.

Neuropathology Studies of Dementia in US Persons other than Non-Hispanic Whites.

Alzheimer's disease (AD) and vascular dementia are two of the most prevalent dementias that afflict the aging population in the United States (US). Studies have made great strides in understanding the neuropathology of these diseases; however, many studies are conducted in the context of non-Hispanic whites (NHWs), and few include the rapidly growing underrepresented populations that reside in the US. We sought to characterize current knowledge of the neuropathologic landscape of AD and vascular dementia of the largest growing US minority groups, namely Latinos/Hispanics, Black Americans, and Asian Americans, compared with NHWs being the majority group. It is vital to note these historic categories are social constructs and cultural and social associations may underlie differences.  We conducted a literature search utilizing specific criteria to yield neuropathology papers that addressed the demographics and neuropathologies of relevance, then collated the findings into this review. We reveal that while there has been much progress in neuropathological research involving Latinos/Hispanics and Black Americans in the past decade, no cohesive conclusions could be extrapolated from the existing data due to the dearth of minority participants and even smaller amount of information related to the heterogeneity within each minority group, especially Latinos/Hispanics. Furthermore, we reveal an even greater scarcity in neuropathological studies involving Asian Americans, also a very heterogeneous group. We hope the presented findings will illuminate the paucity of minority representation in not just neuropathological research but the field of clinical research overall and serve to inspire clinicians and researchers to help reduce the health disparities underrepresented groups in the US face.

Leptin Attenuates Cardiac Hypertrophy in Patients With Generalized Lipodystrophy.

CONTEXT: Lipodystrophy syndromes are rare disorders of deficient adipose tissue, low leptin, and severe metabolic disease, affecting all adipose depots (generalized lipodystrophy, GLD) or only some (partial lipodystrophy, PLD). Left ventricular (LV) hypertrophy is common (especially in GLD); mechanisms may include hyperglycemia, dyslipidemia, or hyperinsulinemia. OBJECTIVE: Determine effects of recombinant leptin (metreleptin) on cardiac structure and function in lipodystrophy. METHODS: Open-label treatment study of 38 subjects (18 GLD, 20 PLD) at the National Institutes of Health before and after 1 (N = 27), and 3 to 5 years (N = 23) of metreleptin. Outcomes were echocardiograms, blood pressure (BP), triglycerides, A1c, and homeostasis model assessment of insulin resistance. RESULTS: In GLD, metreleptin lowered triglycerides (median [interquartile range] 740 [403-1239], 138 [88-196], 211 [136-558] mg/dL at baseline, 1 year, 3-5 years, P < .0001), A1c (9.5 ±â€…3.0, 6.5 ±â€…1.6, 6.5 ±â€…1.9%, P < .001), and HOMA-IR (34.1 [15.2-43.5], 8.7 [2.4-16.0], 8.9 [2.1-16.4], P < .001). Only HOMA-IR improved in PLD (P < .01). Systolic BP decreased in GLD but not PLD. Metreleptin improved cardiac parameters in patients with GLD, including reduced posterior wall thickness (9.8 ±â€…1.7, 9.1 ±â€…1.3, 8.3 ±â€…1.7 mm, P < .01), and LV mass (140.7 ±â€…45.9, 128.7 ±â€…37.9, 110.9 ±â€…29.1 g, P < .01), and increased septal e' velocity (8.6 ±â€…1.7, 10.0 ±â€…2.1, 10.7 ±â€…2.4 cm/s, P < .01). Changes remained significant after adjustment for BP. In GLD, multivariate models suggested that reduced posterior wall thickness and LV mass index correlated with reduced triglycerides and increased septal e' velocity correlated with reduced A1c. No changes in echocardiographic parameters were seen in PLD. CONCLUSION: Metreleptin attenuated cardiac hypertrophy and improved septal e' velocity in GLD, which may be mediated by reduced lipotoxicity and glucose toxicity. The applicability of these findings to leptin-sufficient populations remains to be determined.

Clinical Significance of Spontaneous Echo Contrast on Extracorporeal Membrane Oxygenation.

BACKGROUND: Spontaneous echo contrast (SEC) is known to be a predisposition to thromboembolism and cerebrovascular accident. The aim of this study was to investigate the risk factors and the consequences of SEC in patients who were placed on venoarterial extracorporeal membrane oxygenation (VA-ECMO) because of cardiogenic shock. METHODS: Between January 2011 and December 2014, 98 patients underwent the insertion of VA-ECMO because of cardiogenic shock in our institution. Transthoracic and transesophageal echocardiography was performed and interpreted by National Board of Echocardiography certified cardiologists. Patients were divided into 2 groups based on the presence or absence of SEC. Clinical data, echocardiographic measurements, and outcomes were compared between the 2 groups. RESULTS: Of the 98 patients, 22 patients (22%) had SEC on echocardiography. Patients in the SEC group had a lower ejection fraction (8.0% versus 29%; p < 0.001), a lower pulsatility index (defined by [systolic blood pressure - diastolic blood pressure]/mean blood pressure) while receiving ECMO (0.13 ± 0.14 versus 0.26 ± 0.22; p = 0.009). The SEC group had a higher rate of intracardiac thrombus (46% versus 13%; p = 0.002) and stroke (36% versus 7.9%; p = 0.002). On univariate analysis, intracardiac thrombus, SEC, and low pulsatility were significant risk factors for the development of stroke. On multivariate analysis, SEC was the only independent risk factor for stroke. CONCLUSIONS: SEC on VA-ECMO resulted in an increased risk of intracardiac thrombus and stroke. Maintaining pulsatility while the patient is on ECMO may result in a decreased chance of developing SEC and stroke.

Cardiomyopathy in becker muscular dystrophy: Overview.

Becker muscular dystrophy (BMD) is an X-linked recessive disorder involving mutations of the dystrophin gene. Cardiac involvement in BMD has been described and cardiomyopathy represents the number one cause of death in these patients. In this paper, the pathophysiology, clinical evaluations and management of cardiomyopathy in patients with BMD will be discussed.

Hypertension crisis in the emergency department.

Hypertensive crises, which include hypertensive emergencies and urgencies, are frequently encountered in the emergency department, and require immediate attention as they can lead to irreversible end-organ damage. Normal blood pressure (BP) regulation is altered during acute rises in BP, leading to end-organ damage. Multiple organs can be injured. Special considerations should be given to hypertensive pregnant patients and patients with postoperative hypertension. Treatment should be individualized to each patient based on the type and extent of end-organ damage, degree of BP elevation, and the specific side effects that each medication could have on a patient's preexisting comorbidities.

Inflammatory and hemostatic response to cardiopulmonary bypass in pediatric population: feasibility of seriological testing of multiple biomarkers.

Perioperative myocardial and cerebral damages are the major determinants of postoperative morbidity and mortality in pediatric cardiac surgery. Cardiopulmonary bypass (CPB) causes alterations in the levels of biomarkers related to inflammation, tissue damage, and other tissue pathologies. Early and accurate evaluation of inflammation and tissue damage would therefore be clinically useful. Our objective is to assess the suitability of using Multi-Analyte Profiling (MAP) (Rules Based Medicine, Austin, TX, USA) in pediatric cardiac surgery as a potential surrogate marker of clinical outcome. MAP technology platform allowed us to analyze 90 different biomarkers using only 100µL of plasma to detect any changes in the levels of 90 biomarkers. Plasma samples (100µL) were collected at five different time points: 1. before midline incision; 2. on CPB for 3-5min; 3. at the end of CPB; 4. 1h after CPB; and 5. 24h after CPB. After removing the outliers, the average and standard deviation of the values obtained from the 10 patients were calculated for each time point. The average values of each biomarker at each time point were then compared to each other and to the baseline. The pilot protocol included 10 patients (ages from 3 months to 4 years old) with similar Jenkins risks stratifications who underwent nonpulsatile CPB. We detected changes in the levels of 90 biomarkers. Biomarkers were assessed in groups. Myeloperoxidase (MPO) and pregnancy-associated plasma protein A (PAPP-A) were the earliest markers to rise with 49- and 18-fold increases 3-5min after the onset of CPB, respectively. The most striking increase was noted in the heart-type fatty acid-binding protein (FABP) levels. FABP increased 25, 193, 151, and 4-fold at time points 2, 3, 4, and 5, respectively. Surges in the novel markers of injury were followed by the markers of inflammation (i.e., C-reactive protein, interleukins) peaking at 24h after CPB. This pilot study shows that it is possible to measure 90 different biomarkers using only a very small sample of plasma to evaluate the effects of CPB. Novel markers of tissue injury (FABP, PAPP-A, or MPO) are the earliest markers to rise. Serial monitoring of multiple biomarkers may help to predict and improve outcomes after pediatric cardiac surgery.

Plasmodial surface anion channel-independent phloridzin resistance in Plasmodium falciparum.

The plasmodial surface anion channel (PSAC) is an unusual ion channel induced on the human red blood cell membrane after infection with the malaria parasite, Plasmodium falciparum. Because PSAC is permeant to small metabolic precursors essential for parasite growth and is present on red blood cells infected with geographically divergent parasite isolates, it may be an ideal target for future antimalarial development. Here, we used chemically induced mutagenesis and known PSAC antagonists that inhibit in vitro parasite growth to examine whether resistance mutations in PSAC can be readily induced. Stable mutants resistant to phloridzin were generated and selected within 3 weeks after treatment with 1-methyl-3-nitro-1-nitrosoguanidine. These mutants were evaluated with osmotic lysis and electrophysiological transport assays, which indicate that PSAC inhibition by phloridzin is complex with at least two different modes of inhibition. Mutants resistant to the growth inhibitory effects of phloridzin expressed PSAC activity indistinguishable from that on sensitive parasites, indicating selection of resistance via mutations in one or more other parasite targets. Failure to induce mutations in PSAC activity is consistent with a highly constrained channel protein less susceptible to resistance mutations; whether this protein is parasite- or host-encoded remains to be determined.