bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dehydration is how you define it: comparison of 318 blood and urine athlete spot checks
Authors: Hew-Butler Tamara D , Eskin Christopher , Bickham Jordan , Rusnak Mario , VanderMeulen Melissa 
Published: February 2018

Clinical medicine defines dehydration using blood markers that confirm hypertonicity (serum sodium concentration ([Na+])>145 mmol/L) and intracellular dehydration. Sports medicine equates dehydration with a concentrated urine as defined by any urine osmolality (UOsm) ≥700 mOsmol/kgH2O or urine specific gravity (USG) ≥1.020.ObjectiveTo compare blood versus urine indices of dehydration in a cohort of athletes undergoing routine screenings.Methods318 collegiate athletes (193 female) provided blood and urine samples and asked to rate how thirsty they were on a 10-point visual analogue scale. Serum was analysed for [Na+], while serum and UOsm were measured using an osmometer. USG was measured using a Chemstrip. Data were categorised into dehydrated versus hydrated groupings based on these UOsm and USG thresholds.ResultsUsing UOsm ≥700 mOsmol/kgH2O to define dehydration, 55% of athletes were classified as dehydrated. Using any USG ≥1.020 to define dehydration, 27% of these same athletes were classified as dehydrated. No athlete met the clinical definition for dehydration (hypertonicity; serum [Na+]>145 mmol/L). Normonatremia (serum [Na+] between 135 mmol/L and 145 mmol/L) was maintained in 99.7% of athletes despite wide variation in UOsm (110–1298 mOsmol/kgH2O). A significant correlation was confirmed between serum [Na+] versus UOsm (r=0.18; P<0.01), although urine concentration extremes did not reflect derangement in serum markers or thirst rating.ConclusionUrine concentration thresholds classified 27%–55% of collegiate athletes as dehydrated, while no athlete was dehydrated according to blood [Na+] measurement. Practitioners should caution against using urine indices to diagnose or monitor dehydration, because urinary output is a response rather than a reflection of (tightly regulated) blood tonicity.
Enhanced patient research participation: a Photovoice study in Blantyre Malawi
Authors: Bates Maya Jane , Ardrey Jane , Mphwatiwa Treza , Squire Stephen Bertel , Niessen Louis Willem 
Published: February 2018

ObjectivesPatient involvement in palliative care research is a desirable if challenging goal. Photovoice is an action research method in which affected communities gather photographs to document and discuss their communities’ strengths and concerns. Engagement with policymakers is a separately stated goal. Photovoice is increasingly used in health-related research but has not been widely described in the palliative care literature. We report on experiences and lessons learnt using Photovoice in Blantyre, Malawi to encourage its wider use in research and practice.MethodsThirteen co-researchers (six patients and seven household carers, mean age 47 years) receiving community-based palliative care, attended nine half-day group sessions over a 4-month period. Co-researchers produced, selected and analysed photographs. On completion of data collection, they conducted an advocacy event, including a photographic exhibition, to which media representatives and community leaders were invited.ResultsProcedures to ensure safety of co-researchers and to obtain consent of individuals identified in the photographs were developed during the planning phase. Co-researchers engaged with the Photovoice process with enthusiasm, although frailty and physical disability (poor sight) limited participation for some older adults. Inclusion of palliative care staff within the research team helped to facilitate open dialogue and clinical review where appropriate.ConclusionsIn this Photovoice study, patients and family members receiving palliative care engaged in an exploration of household well-being using photography, participatory analysis and an advocacy event. With appropriate planning, Photovoice can be adapted to a range of settings to enhance patient participation.
Socioeconomic inequality in recovery from poor physical and mental health in mid-life and early old age: prospective Whitehall II cohort study
Authors: Tanaka Akihiro , Shipley Martin J , Welch Catherine A , Groce Nora E , Marmot Michael G , Kivimaki Mika , Singh-Manoux Archana , Brunner Eric J 
Published: February 2018

BackgroundFew studies have examined the influence of socioeconomic status on recovery from poor physical and mental health.MethodsProspective study with four consecutive periods of follow-up (1991–2011) of 7564 civil servants (2228 women) recruited while working in London. Health was measured by the Short-Form 36 questionnaire physical and mental component scores assessed at beginning and end of each of four rounds. Poor health was defined by a score in the lowest 20% of the age–sex-specific distribution. Recovery was defined as changing from a low score at the beginning to a normal score at the end of the round. The analysis took account of retirement status, health behaviours, body mass index and prevalent chronic disease.ResultsOf 24 001 person-observations in the age range 39–83, a total of 8105 identified poor physical or mental health. Lower grade of employment was strongly associated with slower recovery from poor physical health (OR 0.73 (95% CI 0.59 to 0.91); trend P=0.002) in age, sex and ethnicity-adjusted analyses. The association was halved after further adjustment for health behaviours, adiposity, systolic blood pressure (SBP) and serum cholesterol (OR 0.85 (0.68 to 1.07)). In contrast, slower recovery from poor mental health was associated robustly with low employment grade even after multiple adjustment (OR 0.74 (0.59 to 0.93); trend P=0.02).ConclusionsSocioeconomic inequalities in recovery from poor physical health were explained to a considerable extent by health behaviours, adiposity, SBP and serum cholesterol. These risk factors explained only part of the gradient in recovery for poor mental health.
Cardiovascular health among the Czech population at the beginning of the 21st century: a 12-year follow-up study
Authors: Lustigova Michala , Dzurova Dagmar , Pikhart Hynek , Kubinova Ruzena , Bobak Martin 
Published: February 2018

BackgroundIn the late 1980s, Czechia was among the countries which had the highest cardiovascular mortality in the world. In spite of enormous improvements since that time, there are still large opportunities in further improving cardiovascular health.MethodsBased on the Czech Health, Alcohol and Psychosocial Factors in Eastern Europe sample (n=8449 at baseline, 12 years of follow-up, 494 cardiovascular disease (CVD) deaths up to 2015—events), the impact of selected covariates such as education, smoking habits, high blood pressure, blood cholesterol level, diabetes, obesity, physical activity and binge drinking and their multifactorial effects on cardiovascular mortality was evaluated by Cox regression. In addition, population attributable fractions (PAFs) were used to quantify the impact of these factors on CVD mortality in the population.ResultsEducation was found as the strongest determinant of CVD mortality (primary vs university, HR 2.77, P<0.001; PAF=50.5%). CVD risk was two times higher for persons with diabetes compared with those without (HR 2.02, P<0.001, PAF=23.2%). Furthermore, significant factors found were smoking (smoker vs non-smoker, HR 1.91, P<0.001; PAF=26.5%), high blood pressure (HR 1.73, P<0.001; PAF=35.3%) and physical inactivity (none vs sufficient, HR 1.60, P<0.001; PAF=22.9%). Conversely, the effect of obesity was low (HR 1.29, P value =0.020), and binge drinking and high blood cholesterol level were not significant at all.ConclusionsEducation had the largest impact on cardiovascular mortality among the Czech population. More than 50% of CVD death would be prevented if the whole population had the same risk values as the highest educated population. Reducing disparities in health related to education should benefit from attention to cardiovascular health literacy.
Early experience with a temporary bridging device (Comaneci) in the endovascular treatment of ruptured wide neck aneurysms
Authors: Sirakov Stanimir , Sirakov Alexander , Hristov Hristo , Minkin Krasimir , Penkov Marin , Karakostov Vasil 
Published: February 2018

BackgroundThe difficulties in obtaining complete and stable endovascular occlusion are most evident for ruptured aneurysms exhibiting a wide neck and unfavorable geometric features. The aim of our study was to presentourexperience with the Comaneci temporary bridging device in ruptured wide neck aneurysms.MethodsFrom May to July 2017, 29 ruptured aneurysms underwent endovascular embolization with the Comaneci device. Angiographic and clinical results were retrospectively analyzed.Results29 ruptured intracranial aneurysms from different locations were included. Successful embolization was achieved in all lesions; complete post-procedure occlusion was seen in 25 (86%) cases. Insufficient embolization or neck remnant was observed in four cases (13.7%). Complications probably related, directly related, or indirectly related to the device occurred in 3.44% of patients (1/29 patients). At least one angiographic follow-up was performed in each of the 29 cases. The 12 month follow-up examination has yet to be done.ConclusionThe Comaneci device offers a new promising and reliable technique that can safely support aneurysm coiling occlusion even in a rupture environment. However, long term monitoring of patients treated by this device is mandatory.
VIP is involved in peripheral CRF-induced stimulation of propulsive colonic motor function and diarrhea in male rats
Authors: Yakabi Seiichi , Wang Lixin , Karasawa Hiroshi , Yuan Pu-Qing , Koike Kazuhiko , Yakabi Koji , Taché Yvette 
Published: February 2018

We investigated whether vasoactive intestinal peptide (VIP) and/or prostaglandins contribute to peripheral corticotropin-releasing factor (CRF)-induced CRF1 receptor-mediated stimulation of colonic motor function and diarrhea in rats. The VIP antagonist, [4Cl-D-Phe6, Leu17]VIP injected intraperitoneally completely prevented CRF (10 µg/kg ip)-induced fecal output and diarrhea occurring within the first hour after injection, whereas pretreatment with the prostaglandins synthesis inhibitor, indomethacin, had no effect. In submucosal plexus neurons, CRF induced significant c-Fos expression most prominently in the terminal ileum compared with duodenum and jejunum, whereas no c-Fos was observed in the proximal colon. c-Fos expression in ileal submucosa was colocalized in 93.4% of VIP-positive neurons and 31.1% of non-VIP-labeled neurons. CRF1 receptor immunoreactivity was found on the VIP neurons. In myenteric neurons, CRF induced only a few c-Fos-positive neurons in the ileum and a robust expression in the proximal colon (17.5 ± 2.4 vs. 0.4 ± 0.3 cells/ganglion in vehicle). The VIP antagonist prevented intraperitoneal CRF-induced c-Fos induction in the ileal submucosal plexus and proximal colon myenteric plexus. At 60 min after injection, CRF decreased VIP levels in the terminal ileum compared with saline (0.8 ± 0.3 vs. 2.5 ± 0.7 ng/g), whereas VIP mRNA level detected by qPCR was not changed. These data indicate that intraperitoneal CRF activates intestinal submucosal VIP neurons most prominently in the ileum and myenteric neurons in the colon. It also implicates VIP signaling as part of underlying mechanisms driving the acute colonic secretomotor response to a peripheral injection of CRF, whereas prostaglandins do not play a role. NEW & NOTEWORTHY Corticotropin-releasing factor (CRF) in the gut plays a physiological role in the stimulation of lower gut secretomotor function induced by stress. We showed that vasoactive intestinal peptide (VIP)-immunoreactive neurons in the ileal submucosal plexus expressed CRF1 receptor and were prominently activated by CRF, unlike colonic submucosal neurons. VIP antagonist abrogated CRF-induced ileal submucosal and colonic myenteric activation along with functional responses (defecation and diarrhea). These data point to VIP signaling in ileum and colon as downstream effectors of CRF.
Altered Achilles tendon function during walking in people with diabetic neuropathy: implications for metabolic energy saving
Authors: Petrovic M. , Maganaris C. N. , Deschamps K. , Verschueren S. M. , Bowling F. L. , Boulton A. J. M. , Reeves N. D. 
Published: February 2018

The Achilles tendon (AT) has the capacity to store and release elastic energy during walking, contributing to metabolic energy savings. In diabetes patients, it is hypothesized that a stiffer Achilles tendon may reduce the capacity for energy saving through this mechanism, thereby contributing to an increased metabolic cost of walking (CoW). The aim of this study was to investigate the effects of diabetes and diabetic peripheral neuropathy (DPN) on the Achilles tendon and plantarflexor muscle-tendon unit behavior during walking. Twenty-three nondiabetic controls (Ctrl); 20 diabetic patients without peripheral neuropathy (DM), and 13 patients with moderate/severe DPN underwent gait analysis using a motion analysis system, force plates, and ultrasound measurements of the gastrocnemius muscle, using a muscle model to determine Achilles tendon and muscle-tendon length changes. During walking, the DM and particularly the DPN group displayed significantly less Achilles tendon elongation (Ctrl: 1.81; DM: 1.66; and DPN: 1.54 cm), higher tendon stiffness (Ctrl: 210; DM: 231; and DPN: 240 N/mm), and higher tendon hysteresis (Ctrl: 18; DM: 21; and DPN: 24%) compared with controls. The muscle fascicles of the gastrocnemius underwent very small length changes in all groups during walking (~0.43 cm), with the smallest length changes in the DPN group. Achilles tendon forces were significantly lower in the diabetes groups compared with controls (Ctrl: 2666; DM: 2609; and DPN: 2150 N). The results strongly point toward the reduced energy saving capacity of the Achilles tendon during walking in diabetes patients as an important factor contributing to the increased metabolic CoW in these patients. NEW & NOTEWORTHY From measurements taken during walking we observed that the Achilles tendon in people with diabetes and particularly people with diabetic peripheral neuropathy was stiffer, was less elongated, and was subject to lower forces compared with controls without diabetes. These altered properties of the Achilles tendon in people with diabetes reduce the tendon’s energy saving capacity and contribute toward the higher metabolic energy cost of walking in these patients.
Intermittent PTH 1–34 administration improves the marrow microenvironment and endothelium-dependent vasodilation in bone arteries of aged rats
Authors: Lee Seungyong , Bice Ashley , Hood Brianna , Ruiz Juan , Kim Jahyun , Prisby Rhonda D. 
Published: February 2018

Inflammation coincides with diminished marrow function, vasodilation of blood vessels, and bone mass. Intermittent parathyroid hormone (PTH) administration independently improves marrow and vascular function, potentially impacting bone accrual. Currently, the influence of marrow and intermittent PTH administration on aged bone blood vessels has not been examined. Vasodilation of the femoral principal nutrient artery (PNA) was assessed in the presence and absence of marrow. Furthermore, we determined the influence of PTH 1–34 on 1) endothelium-dependent vasodilation and signaling pathways [i.e., nitric oxide (NO) and prostacyclin (PGI2)], 2) endothelium-independent vasodilation, 3) cytokine production by marrow cells, and 4) bone microarchitecture and bone static and dynamic properties. Young (4–6 mo) and old (22–24 mo) male Fischer-344 rats were treated with PTH 1–34 or a vehicle for 2 wk. In the absence and presence of marrow, femoral PNAs were given cumulative doses of acetylcholine, with and without the NO and PGI2blockers, and diethylamine NONOate. Marrow-derived cytokines and bone parameters in the distal femur were assessed. Exposure to marrow diminished endothelium-dependent vasodilation in young rats. Reduced bone volume and NO-mediated vasodilation occurred with old age and were partially reversed with PTH. Additionally, PTH treatment in old rats restored endothelium-dependent vasodilation in the presence of marrow and augmented IL-10, an anti-inflammatory cytokine. Endothelium-independent vasodilation was unaltered, and PTH treatment reduced osteoid surfaces in old rats. In conclusion, the marrow microenvironment reduced vascular function in young rats, and PTH treatment improved the marrow microenvironment and vasodilation with age.NEW & NOTEWORTHY This study investigated the influence of the marrow microenvironment on bone vascular function in young and old rats. An inflamed marrow microenvironment may reduce vasodilator capacity of bone blood vessels, diminishing delivery of blood flow to the skeleton. In young rats, the presence of the marrow reduced vasodilation in the femoral principal nutrient artery (PNA). However, intermittent parathyroid hormone administration (i.e., a treatment for osteoporosis) improved the marrow microenvironment and vasodilator capacity in old PNAs.
Surface electromyographic amplitude does not identify differences in neural drive to synergistic muscles
Authors: Martinez-Valdes Eduardo , Negro Francesco , Falla Deborah , De Nunzio Alessandro Marco , Farina Dario 
Published: February 2018

Surface electromyographic (EMG) signal amplitude is typically used to compare the neural drive to muscles. We experimentally investigated this association by studying the motor unit (MU) behavior and action potentials in the vastus medialis (VM) and vastus lateralis (VL) muscles. Eighteen participants performed isometric knee extensions at four target torques [10, 30, 50, and 70% of the maximum torque (MVC)] while high-density EMG signals were recorded from the VM and VL. The absolute EMG amplitude was greater for VM than VL ( P < 0.001), whereas the EMG amplitude normalized with respect to MVC was greater for VL than VM ( P < 0.04). Because differences in EMG amplitude can be due to both differences in the neural drive and in the size of the MU action potentials, we indirectly inferred the neural drives received by the two muscles by estimating the synaptic inputs received by the corresponding motor neuron pools. For this purpose, we analyzed the increase in discharge rate from recruitment to target torque for motor units matched by recruitment threshold in the two muscles. This analysis indicated that the two muscles received similar levels of neural drive. Nonetheless, the size of the MU action potentials was greater for VM than VL ( P < 0.001), and this difference explained most of the differences in EMG amplitude between the two muscles (~63% of explained variance). These results indicate that EMG amplitude, even following normalization, does not reflect the neural drive to synergistic muscles. Moreover, absolute EMG amplitude is mainly explained by the size of MU action potentials. NEW & NOTEWORTHY Electromyographic (EMG) amplitude is widely used to compare indirectly the strength of neural drive received by synergistic muscles. However, there are no studies validating this approach with motor unit data. Here, we compared between-muscles differences in surface EMG amplitude and motor unit behavior. The results clarify the limitations of surface EMG to interpret differences in neural drive between muscles.
Essential Role of Polo-like Kinase 1 (Plk1) Oncogene in Tumor Growth and Metastasis of Tamoxifen-Resistant Breast Cancer
Authors: Jeong Sung Baek , Im Ji Hye , Yoon Jeong-Hoon , Bui Quyen Thu , Lim Sung Chul , Song Joon Myong , Shim Yumi , Yun Jieun , Hong Janghee , Kang Keon Wook 
Published: February 2018

AbstractThe most common therapy for estrogen receptor–positive breast cancer is antihormone therapy, such as tamoxifen. However, acquisition of resistance to tamoxifen in one third of patients presents a serious clinical problem. Polo-like kinase 1 (Plk1) is a key oncogenic regulator of completion of G2–M phase of the cell cycle. We assessed Plk1 expression in five chemoresistant cancer cell types and found that Plk1 and its downstream phosphatase Cdc25c were selectively overexpressed in tamoxifen-resistant MCF-7 (TAMR-MCF-7) breast cancer cells. Real-time monitoring of cell proliferation also showed that TAMR-MCF-7 cells were more sensitive to inhibition of cell proliferation by the ATP-competitive Plk1 inhibitor BI2536 than were the parent MCF-7 cells. Moreover, BI2536 suppressed expression of epithelial–mesenchymal transition marker proteins and 3D spheroid formation in TAMR-MCF-7 cells. Using TAMR-MCF-7 cell–implanted xenograft and spleen–liver metastasis models, we showed that BI2536 inhibited tumor growth and metastasis in vivo. Our results suggest that Plk1 could be a novel target for the treatment of tamoxifen-resistant breast cancer. Mol Cancer Ther; 17(4); 825–37. ©2018 AACR.
Multi-omics Approach Reveals Distinct Differences in Left- and Right-Sided Colon Cancer
Authors: Hu Wangxiong , Yang Yanmei , Li Xiaofen , Huang Minran , Xu Fei , Ge Weiting , Zhang Suzhan , Zheng Shu 
Published: February 2018

Abstract
Increasing evidence suggests that left-sided colon cancer (LCC) and right-sided colon cancer (RCC) are emerging as two different colorectal cancer types with distinct clinical characteristics. However, the discrepancy in the underlying molecular event between these types of cancer has not been thoroughly elucidated to date and warrants comprehensive investigation. To this end, an integrated dataset from The Cancer Genome Atlas was used to compare and contrast LCC and RCC, covering mutation, DNA methylation, gene expression, and miRNA. Briefly, the signaling pathway cross-talk is more prevalent in RCC than LCC, such as RCC-specific PI3K pathway, which often exhibits cross-talk with the RAS and P53 pathways. Meanwhile, methylation signatures revealed that RCC was hypermethylated relative to LCC. In addition, differentially expressed genes (n = 253) and differentially expressed miRNAs (n = 16) were determined between LCC and RCC. Especially for Prostate Cancer Susceptibility Candidate 1 (PRAC1), a gene that was closely associated with hypermethylation, was the top significantly downregulated gene in RCC. Multi-omics comparison of LCC and RCC suggests that there are more aggressive markers in RCC and that tumor heterogeneity occurs within the location-based subtypes of colon cancer. These results clarify the debate regarding the conflicting prognosis between LCC and RCC, as proposed by different studies.
Implications: The underlying molecular features present in LCC and RCC identified in this study are beneficial for adopting reasonable therapeutic approaches to prolong overall survival and progression-free survival in colorectal cancer patients. Mol Cancer Res; 16(3); 476–85. ©2017 AACR.