bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gestational dependent responses to second hand smoke (SHS) in mouse pregnancies
Authors: Wendt Ryan , Stapley Brendan , Clark Evan , Curtis Katrina , Clarke Derek , Reynolds Paul , Arroyo Juan 
Published: May 2023

Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights leading to the development of intrauterine growth restriction (IUGR) in mice. Hypertension and proteinuria are two important hallmarks of obstetric pathology leading to the development of preeclampsia (PE). In the present study, we wanted to determine the effects SHS exposure at two different important gestational points during mouse pregnancy. C57/Bl6 mice were exposed to SHS via a nose-only delivery system (Scireq) for 4 days (from 14.5 gestational day (dGA) to 17.5 dGA) or for 6 days (from 12.5 dGA to 17.5 dGA). At the time of necropsy (18.5 dGA) placental and fetal weights were recorded. Maternal blood pressure was determined with a tail occlusion cuff (Kent Scientific) and dip stick test for proteinuria was obtained. Treatment with SHS showed: 1) a significant decrease in placental weight (p<0.0001) and fetal weight (p<0.0002) following 4 days of exposure, 2) higher systolic (p<0.02) and diastolic (p<0.02) blood pressure following 6 days of exposure, and 3) increased proteinuria after 6 days of exposure. We conclude that detrimental effects of SHS coincides with the length of maternal exposure. We confirmed that 4 days of exposure resulted in metrics common to IUGR while 6 days of exposure more closely resembled PE pathology. These results could be beneficial in understanding the long-term effects of SHS exposure and the development of placental diseases. NIH 1R15HD108743 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Identification of Molecular Markers of Diabetic Foot Ulcer Severity
Authors: Flores Mario , Flores Mario , Paniagua Karla 
Published: May 2023

Diabetes prevalence estimates in South Texas exceeds national estimates and diagnosed cases are higher among Hispanic adults compared to their non-Hispanic white counterparts. San Antonio, a predominantly Hispanic city reports significantly higher annual rates of diabetic amputations compared to Texas. Late identification of severe foot ulcers minimizes the likelihood of reducing amputation risk. In this study we investigate the use of a deep learning pipeline for single cell transcriptomics to identify key markers for Diabetic Foot Ulcer (DFU) severity and progression that can help prioritize individuals with high-risk of foot ulcer amputation. We observed substantial differences in cell types as well as transcripts of patients classified as non-DFU, DFU healers, DFU non-healers compared to healthy individuals. In particular cell sub-type composition show significant differences in DFU non-healers compared to non-DFU and DFU healers. As an indicator of immune defense, populations of T cells accounted for 5.26% in the non-healer group and decreased to 1.17% in the healer group. To obtain more insights into the molecular markers of severity, we developed a graph convolutional neural network (GCNN) model. We observed that the GCNN model reach a prediction accuracy of the severity of 90.32%. Overall, our study indicates significant differences in the gene expression profiles of inflammatory response and immune cells of non-healer patients. The identification of individuals with high risk of amputations is important to maintain the quality of life and thus has significant social-economic impact. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Esophageal expression of Na+/H+ exchanger 2 and -3 (nhe2 and -3) gene transcripts in Atlantic salmon during smoltification and seawater acclimation
Authors: Richardson Sierra , Runiewicz Ellie , Bradley Serena , Hall Daniel , McCormick Stephen , Breves Jason 
Published: May 2023

Atlantic salmon ( Salmo salar) undergo smoltification, a springtime transformation associated with the development of physiological, morphological, and behavioral traits that enable individuals to thrive in pelagic marine habitats. In particular, the capacity for salmon to maintain hydromineral balance in seawater is attained through the coordinated development of ion- and water-transporting processes in key organs such as the gill, kidney, and gastrointestinal tract. To combat dehydration, Atlantic salmon drink ambient seawater that is initially desalinated in the esophagus to enable subsequent solute-linked water absorption by the intestine. The molecular processes underlying esophageal desalination of imbibed seawater and their regulation during smoltification and following seawater exposure remain largely unresolved. The current study explored whether Na+/H+ exchangers in the esophagus may contribute to the removal of Na+ from luminal seawater. We first determined that both nhe2 and -3 were robustly expressed in the esophagus of smolts; nhe2 was also highly expressed in gill and stomach. Next, we sampled salmon undergoing smoltification and observed springtime elevations in branchial Na+/K+-ATPase activity, Na+/K+/2Cl- cotransporter 1 and cystic fibrosis transmembrane regulator 1 transcription that coincided with increased seawater tolerance. There were no parallel springtime changes in esophageal nhe2 or -3 expression; but nhe3 expression was enhanced in smolts after 2 days of seawater exposure. In a subsequent experiment, we observed elevated nhe2 and -3 expression in smolts that were long-term acclimated (2 weeks) to seawater versus freshwater. Collectively, our results indicate that Na+/H+ exchangers contribute to the desalination processes in the esophagus. The next challenge will be to determine whether essential “seawater-adapting hormones,” such as growth hormone and cortisol, regulate the expression of Na+/H+ exchangers in support of seawater acclimation. Supported by the National Science Foundation (IOS-1755131 to J.P.B.). National Science Foundation [IOS-1755131] This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Lipoprotein lipase underlies the vascular anti-contractile effect of perivascular adipose tissue (PVAT)
Authors: Corley Scott , Costa Tiago , Wilson Emily , Waigi Emily , Wenceslau Camilla , McCarthy Cameron 
Published: May 2023

Physiologically, perivascular adipose tissue (PVAT) exerts an anti-contractile effect on the vasculature. This effect is mediated by the biosynthesis and liberation of a myriad of anti-contractile molecules (e.g., adipokines). However, this anti-contractile function generally is lost with aging and cardiovascular diseases such as hypertension and diabetes. Lipoprotein lipase (LPL) is an enzyme classically known for hydrolyzing triglycerides into free fatty acids and glycerol. However, it is unknown whether LPL underlies the anti-contractile effect of PVAT. Specifically, we hypothesized that by inhibiting lipoprotein lipase (LPL) activity with Atglistatin, we would abolish the anti-contractile effect of PVAT. To test this hypothesis, mesenteric resistance arteries (MRA), with and without PVAT, were isolated from 3-month-old male Wistar rats and mounted on a wire myograph. Phenylephrine concentration-response curves were performed with and without Atglistatin (10-5M). As expected, PVAT exerted a significant anti-contractile effect on phenylephrine-induced contraction [Emax (mN), -PVAT-vehicle: 18.1±3.0 vs. +PVAT-vehicle: 7.1±1.1, p<0.05]. Incubation of MRA with intact PVAT with Atglistatin significantly increased contraction [Emax (mN), +PVAT-vehicle: 7.1±1.1vs. +PVAT-Atglistatin: 22.6±4.2, p<0.05], suggesting that LPL is indeed important for the anti-contractile effect of PVAT. Crucially, no difference was observed with Atglistatin in MRA lacking PVAT [Emax (mN), -PVAT-vehicle: 18.1±3.0 vs. -PVAT-Atglistatin: 18.5±2.9, p>0.05], indicating that Atglistatin was not increasing contraction via non-PVAT-dependent mechanisms. Overall, these data suggest that LPL is an important mechanism mediating the anti-contractile effect of PVAT and that reduced LPL activity could be contributing to pro-contractile PVAT in aging and cardiovascular diseases. NHLBI (R00HL151889), NIGMS (1P20GM103641 - Pilot Project), UofSC SOM (Startup funds) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Deletion of PREX1 (Phosphatidylinositol-3,4,5-Trisphosphate Dependent Rac Exchange Factor 1) worsens salt sensitive hypertension and kidney damage in Dahl S rats
Authors: Liao Jenny , Liao Tang-Dong , Haque Mohammed , Ortiz Pablo 
Published: May 2023

Prex1 (Phosphatidylinositol 3,4,5-trisphosphate-dependent RAC exchanger 1) is a Rac-specific guanine nucleotide exchanging factor and an integrator of signaling between Rac1 and protein kinase A (PKA). Both Rac1 and PKA are involved in pathways associated with salt sensitive hypertension. However, the roe of Prex1 in renal function and salt sensitive hypertension has not been studied. To investigate the role of Prex1 in salt sensitive hypertension. We used a Prex1 knockout (KO) rat on the Dahl salt sensitive genetic background generated by the RGERC at the Medical College of Wisconsin. Genotyping showed that the Prex1 gene was deleted. We studied the expression and localization of Prex1 in kidney sections using immunolabeling and confocal microscopy. Prex1 protein was mainly located in renal tubules, infiltrating inflammatory cells, and endothelial cells of large vessels. We then studied if deletion of Prex1 altered salt sensitivity of blood pressure. We found that both male and female WT Dahl S and Prex1 KO developed salt sensitivity after 2 weeks of 4% high salt diet. However, the increase in blood pressure was higher in male Prex1 KO Dahl S rats (Prex1 KO: 33± 7, vs male WT: 19± 2 mmHg, p<0.05). In females Prex1 KO, high salt increased BP by 31± 3 mmHg whereas the increase was lower in female WT Dahl S (17± 1 mmHg, p<0.05). Rats were placed in metabolic cages for urine collection. Male rats had increased albuminuria after high salt diet for 2 weeks that was not different between WT and Prex1 KO. Female rats had a smaller increase in albuminuria which was not different between WT and KO. Given the expression of Prex1 in inflammatory cells we quantified macrophage infiltration in the kidney after high salt diet. Male Prex1 KO rats had significantly higher macrophage infiltration compared to WT (WT: 141±10 vs Prex1 KO: 337± 18, p<0.05). Female Prex1 KO rats also had higher macrophage infiltration after high salt diet, but the total number of macrophages was lower than males (103 ± 7 female WT vs 208 ± 18 female Prex1 KO). We conclude that Prex1 protects against salt sensitive hypertension and inflammatory cell infiltration in Dahl salt sensitive rats such that its deletion worsens both phenotypes. Females Dahl S were somewhat protected against salt induced hypertension and this response was not worsened in Prex1 KO. Future experiments will study the role of Prex1 in renal NaCl transport. NIDDK-R56DK131114 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Life science & interpreting students: an interdisciplinary healthcare role-playing activity
Authors: Halpin Patricia , Shaffer Laurie 
Published: May 2023

Objective – Communication is essential to patient care. When serving Deaf patients, medical professionals who work with interpreters provide greater access to healthcare and wellness. Both the medical professional and the interpreter need training to develop the confidence and skills that support successful communication. This study aimed to introduce both Life Sciences and American Sign Language/English Interpreting undergraduate students to the experience of working together via role-play activities designed to promote effective communication with Deaf patients. Students from an Interpreting in the Healthcare Setting course were combined with students from an Endocrinology course to take part in this interdisciplinary assignment. Method – A group of three students per clinic completed each of the role play activities which were designed to simulate common interactions with medical professionals. The Life Science students enacted the role of the medical professional while one of the Interpreting students enacted the role of interpreter and the second enacted the role of a Deaf patient. Separate classrooms were designated as clinics where the role play was enacted. Clinics were designated as primary care intake, emergency department admissions, diabetes clinic and cardiac clinic. A mixed method approach was used to design both qualitative and quantitative questions on pre and post surveys distributed to 18 participants. The qualitative data was analyzed via collaborative review and categorized by theme. Quantitative Likert scale data was collected and analyzed to measure student preparedness, confidence and effectiveness of the activities. Results – The level of preparedness varied with each student and clinic type. All student participants from both courses reported increased confidence and ability when working with each other and with future Deaf patients. Conclusion – The study sought to create an authentic learning experience for undergraduate students who aspired to work in healthcare either as medical professionals or interpreters. By beginning such education earlier in students’ academic careers should result in more robust access to healthcare for Deaf patients. The model we created and evaluated can be used at all levels from community college through professional school to train Life Science students interested in health professions to provide equitable access to healthcare. For Interpreting students, the healthcare setting has a shortage of trained interpreters, and this model can provide them with the needed experience prior to working as interpreters in the healthcare setting. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Arterial Baroreflex Control of Heart Rate in Patients with Chronic Kidney Disease
Authors: Li Sabrina , Jeong Jinhee , Sabino-Carvalho Jeann , DaCosta Dana , Park Jeanie 
Published: May 2023

Chronic kidney disease (CKD) patients have greater blood pressure reactivity to acute cardiovascular stressors and a higher prevalence of hypertension; however, limited information is available regarding the potential role of impaired baroreflex control in non-dialysis CKD patients. The baroreflex plays a homeostatic role in beat-to-beat blood pressure (BP) regulation and impaired cardiac baroreflex sensitivity (cBRS) has been associated with increased blood pressure reactivity and cardiovascular events. However, previous studies in CKD have shown mixed results or have been confounded with co-morbid conditions such as hypertension. Therefore, the aim of the present study was to test the hypothesis that baroreflex control of heart rate (HR) is attenuated in patients with CKD compared to hypertensive controls. Additionally, we tested whether cardiovascular risk factors such as age, arterial stiffness, and BMI are associated with cBRS in patients with CKD. In 15 stage III-IV CKD patients [7 male/8 female, age: 60±10 yr, 14 Black/1 White, systolic/diastolic BP: 145.1±20/71.9 ± 10 mmHg, 100% hypertensive, BMI: 31±5 kg/m2] and 5 matched controls [5 male/0 female, age: 56 ± 4 yr, 5 Black/0 White, systolic/diastolic BP: 130.6± 24/69.0 ±15 mmHg, 100% hypertensive, BMI: 34±4 kg/m2], continuous beat-to-beat BP (finger photoplethysmography) and HR (electrocardiography) were recorded while resting supine for 5-minutes. We utilized the sequence technique in which the slopes of the systolic BP and RR interval relationships were calculated and averaged for a measure of cBRS. Arterial stiffness was measured by carotid-to-femoral pulse wave velocity (PWV) using tonometry. Systolic beat-to-beat BP (CKD 145.1±20 vs. CT 130.6± 24 mmHg, P = 0.184) and HR (CKD 64.2 ± 7 vs. CT 67.5 ± 6 beats/min, P = 0.352) were similar between groups. Likewise, no differences in spontaneous cBRSall (CKD 10.495 ± 5 vs. CT 8.800 ± 3 ms/mmHg, P = 0.487), cBRSup (CKD 9.138 ± 5 vs. CT 9.776 ± 3 ms/mmHg, P = 0.778) and cBRSdown (CKD 11.238 ± 6 vs. CT 8.218 ± 3 ms/mmHg, P = 0.267) were observed. No significant correlations were observed between cBRS with age, BMI, PWV, or eGFR. In summary, contrary to our hypothesis, our preliminary data suggest that CKD does not worsen cBRS compared to age- and co-morbidity-matched controls, but greater sample size is needed to support our results. Funded by American Physiological Society, NIH R01HL135183, NIH R61 AT10457, and VA Merit I01CX001065. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Spontaneous baroreflex control of sympathetic nerve activity and heart rate in young adults with major depressive disorder
Authors: Dominguez Cynthia , Darling Ashley , Skow Rachel , Young Benjamin , Saunders Erika , Fadel Paul , Greaney Jody 
Published: May 2023

Blunted cardiac baroreflex sensitivity is evident in middle-aged adults with depression in remission and likely contributes to increased cardiovascular disease morbidity and mortality. In young adults with major depressive disorder (MDD), there is some evidence that sympathetic outflow at rest is elevated and graded in relation to depressive symptom severity; however, few studies have examined arterial baroreflex function in young adults with MDD. Here, we tested the hypotheses that spontaneous baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) would both be attenuated in young adults with symptomatic MDD (unmedicated) compared to healthy non-depressed adults (HA). Nine HA (22±3 yrs; 6 female) and 10 adults with symptomatic MDD of moderate severity [21±5 yrs; 8 female; 15±3 on the Patient Health Questionnaire-9 (possible score range: 0-27)] participated. MSNA (peroneal microneurography), HR (electrocardiogram), and beat-to-beat blood pressure (BP; finger photoplethysmography) were continuously measured during 10 min of supine rest. To determine spontaneous sympathetic baroreflex gain, weighted linear regression analyses between spontaneous changes in MSNA and diastolic BP (3 mmHg bins) were performed. To estimate spontaneous cardiac baroreflex gain, the relation between systolic BP and R-R interval was determined using the sequence technique. At rest, there were no group differences in MSNA burst incidence (28±10 HA vs. 21±10 bursts/100 heartbeats MDD; p=0.19), HR (62±9 HA vs. 69±11 bpm MDD; p=0.13), or mean arterial pressure (81±6 HA vs. 82±5 mmHg MDD; p=0.70). Sympathetic baroreflex gain was not different between HA and MDD (-3.4±0.8 HA vs. -3.0±1.5 bursts/100 heartbeats/mmHg MDD; p=0.53). There were also no differences in overall cardiac baroreflex gain between groups (24±11 HA vs. 19±6 ms/mmHg MDD; p=0.24). Likewise, there were no group differences in cardiac baroreflex gain when derived separately during either BP rises or BP falls (both p>0.05). These preliminary data demonstrate that spontaneous baroreflex control of both MSNA and HR are preserved in young adults with symptomatic MDD, suggesting that impairments in baroreflex function in adults with depression may only manifest later in the disease trajectory. NIH R21MH123928 and R00 HL133414 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Sympathetic and blood pressure reactivity to acute stress in young adults with major depressive disorder: the influence of depressive symptomatology
Authors: Darling Ashley , Young Benjamin , Skow Rachel , Dominguez Cynthia , Saunders Erika , Fadel Paul , Greaney Jody 
Published: May 2023

Major depressive disorder (MDD) is episodic in nature, highly recurrent, and associated with increased cardiovascular disease (CVD) risk. Sympathetic overactivation in response to acute stress may contribute to MDD-CVD comorbidity. However, few studies have investigated acute sympathetic stress reactivity in young adults with MDD or considered the potential influence of depressive symptom severity on these responses. We hypothesized that 1) acute stress-induced increases in muscle sympathetic nerve activity (MSNA) and blood pressure (BP) would be greater in young adults with MDD (unmedicated) compared to healthy non-depressed adults (HA) and 2) the magnitude of responsiveness would be graded in relation to symptom severity. Twenty-nine HA (22±5 yrs; 17 female) and 40 adults with MDD having mild-to-moderately severe depressive symptoms (23±6 yrs; 32 female) participated. Adults with MDD were also subclassified as having either low (l-MDD, n=25) or high symptom severity (h-MDD, n=15). MSNA (microneurography) and beat-to-beat BP (photoplethysmography) were measured at rest and during the cold pressor test (CPT) and the Stroop color word test (SCWT). There were no group differences in either resting MSNA (17±9 HA vs. 14±6 bursts/min MDD, p=0.39) or mean arterial pressure (MAP; 86±6 HA vs. 84±5 mmHg MDD, p=0.25). The CPT elicited increases in MSNA and MAP (both p<0.01), but the magnitude was not different between groups (MSNA: Δ24±12 HA vs. Δ19±9 bursts/min MDD, p=0.22; MAP: Δ24±8 HA vs. Δ23±9 mmHg MDD, p=0.45). The SCWT also elicited increases in MAP (p<0.01) that were not different between groups (Δ10±7 HA vs Δ10±6 mmHg MDD; p=0.76). Surprisingly, the SCWT failed to cause increases in MSNA (p>0.05), which also did not differ between groups (Δ-2±7 HA vs. Δ-2±8 bursts/min MDD, p=0.92). When further classifying adults with MDD into symptom severity subgroups, there likewise were no differences in MSNA reactivity to either acute stressor (both p>0.05). Interestingly, adults with h-MDD exhibited greater increases in MAP than adults with l-MDD during the CPT (Δ28±9 h-MDD vs. Δ20±8 mmHg l-MDD, p<0.01) but not during the SCWT (Δ9±4 h-MDD vs. Δ11±7 mmHg l-MDD, p=0.63). Contrary to our hypothesis, these data demonstrate that neither acute stress-induced sympathetic activation nor the ensuing increase in BP are exaggerated in young adults with MDD. However, the severity of active depressive symptomatology may influence BP reactivity to generalized stress stimuli, thereby influencing CVD risk profiles. NIH R21MH123928 and R00 HL133414 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.