bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Sleep Apnea in Chronic Kidney Disease
Authors: Pace Carolyn , Riggs Jennifer , Danielson Leslie , Fischer Edgar , Howard Tamara , Kanagy Nancy 
Published: November 2023

Patients with chronic kidney disease (CKD) have increased incidence of sleep apnea compared to those without renal disease. We hypothesized that the hypoxia of sleep apnea accelerates declines in renal function and so might contribute to this association. In our model of CKD (0.4% adenine diet for 3 to 5 weeks), rats developed crystalline nephropathy and elevated blood urea nitrogen (BUN) values (> 140 mg/dl). After return to a normal rat diet, BUN decreased to a stable but still elevated level of 50–70 mg/dl simulating CKD (normal rat BUN = 20 mg/dl). 24‐hour urine volumes were also significantly elevated (CKD = 38±3 vs Control = 9.4±0.5 ml). Urinary protein excretion increased in the adenine diet rats but not in the control diet rats. Rats were then exposed during their sleep period to either intermittent hypoxia (IH) to simulate sleep apnea or sham conditions for six weeks. At the end of the IH or sham exposures, BUN levels were greater in CKD rats exposed to IH compared to Sham conditions (Sham = 78.3±3.7 vs. IH = 91.5±3.1 mg/dl) but were not different in non‐CKD groups. Creatinine clearance was lower in rats exposed to IH for both CKD rats (Sham = 1.0±0.2 vs. IH = 0.81±0.1 ml/min) and in control rats (Sham = 4.2±0.7 vs. IH = 1.6±0.1 ml/min) suggesting IH impairs glomerular function. Histological analysis of kidney sections revealed fibrosis and infiltrates in the regions of the proximal and distal tubules with effaced proximal tubules and decreased total number of tubules in all adenine fed rats. This damage persisted 8 weeks after cessation of the diet, independent of sham or IH exposure. Therefore, an adenine diet causes sustained CKD even after the diet is discontinued that results in polyuria and proteinuria. Exposure to IH further compromises renal function suggesting treating sleep apnea in CKD patients should help to preserve renal filtration function.Support or Funding InformationDialysis Clinic, Inc. (DCI)
Does Exposure to Nanoparticles Alter the Resistance of Bacteria to Antibiotics and Heavy Metals?
Authors: Paek Ashley , Smith Virginia 
Published: November 2023

Titanium dioxide (TiO2) nanoparticles demonstrate the properties of high refractive index and brightness and therefore, are regularly used as reflective optical coats or as whitening pigments. In addition, TiO2 is also used extensively in cosmetics, skin care and sunscreen products due to its transparent appearance under visible light. As the applications for nanoparticles (NP) increase, it is becoming more urgent to understand the levels and mechanisms of their toxicity. Previous work in our lab, and others, has determined that while high levels of NP are toxic to bacteria, low levels of NP actually enhance bacterial growth rates (hormesis). Recent studies have shown that the expression of heavy‐metal and antibiotic efflux pumps is upregulated in response to exposure to nanoparticles. In order to see if such upregulation was responsible for the hormesis observed in our lab, we developed and performed disk diffusion assays on NP‐treated bacterial cultures. Paper disks that had been pre‐treated with different classes of antibiotics or types of metal ions were placed on agar plates containing cultures of E.coli that had either been exposed to nanoparticles or had not. The plates were then incubated overnight to allow the contents of the disk to diffuse into the surrounding agar. Preliminary results indicate that exposure to nanoparticles confers minimal, if any, resistance to ampicillin or lead, nickel, or zinc metal ions. Ongoing tests are investigating other antibiotics, metal ions, and levels of nanoparticle exposure.Support or Funding InformationDefense Threat Research Agency
Markers of Muscle Protein Synthesis and Breakdown in Fast‐Twitch Skeletal Muscle of Rodents Aged 3 to 24 Months
Authors: Mumford Petey W. , Mobley C. Brooks , Kephart Wesley C. , Haun Cody T. , Holland A. Maleah , Osburn Shelby C. , Beck Darren T. , Martin Jeffery M. , Young Kaelin C. , Kavazis Andreas N. , Lowery Ryan P. , Wilson Jake M. , Roberts Michael D. 
Published: November 2023

OBJECTIVEMuscle protein synthesis (MPS) and muscle protein degradation (MPD) are well known modulators for muscle mass maintenance. Given that fast‐twitch skeletal muscle atrophies with aging, we sought to examine the effects of aging on MPS and MPD markers in the plantaris muscle of rodents ranging from 3 to 24 months.MEHTODSMale Fischer 344 rats (300–600g) were successfully aged to 3, 6, 12, 18 and 24 months, were injected with puromycin (0.02 mg/g body mass), euthanized, plantaris muscle was extracted and wet skeletal muscle weights were obtained. Muscle tissue was then processed for biochemical processing. MPS was assessed via the SUNsET method, and MPD was assessed using whole lane densitometry via ubiquitin immunoblotting.RESULTSRelative plantaris masses revealed significant between‐group differences throughout the lifespan (p<0.001); specifically, masses were 18% greater in 3 versus 18 month old rats (p<0.001) and 23% greater in 3 versus 24 month old rats (p<0.001). Interestingly, MPS levels did not differ between 3 month old rats versus all other age groups. However, MPS levels were 2.42‐fold greater in 18 month old versus 24 month old rats (p<0.05). Poly‐ubiquinated protein levels were not different between any of the age groups.CONCLUSIONIt appears that plantaris muscle atrophy occurs with aging. However, this does not appear to be reflected via decrements in MPS or increases in protein polyubiquination. Mechanisms related to fast‐twitch skeletal muscle atrophy remain to be determined and should be further investigated.Support or Funding InformationThis study was supported in part by a contract from The University of Tampa (to M.D.R. from J.M.W.) as well as laboratory start‐up funds from M.D.R.
Enhancement of neural regeneration and functional recovery via DAPK1 suppression in stroke animal model
Authors: Won Jinyoung , Hong Yonggeun 
Published: November 2023

Stroke is the most frequent worldwide cause of adult death. Recently, studies reported an intimate relation between DAPK1 as key player in multiple cell death and ischemic brain injury. We investigated the effect of DAPK1 on neural regeneration and functional recovery following ischemic injury using by Oxazolone, a synthesized DAPK inhibitor. In ischemic stroke model, subjected animals exhibited neurologic damage and altered behavioral outcome. However, suppression of DAPK1 enhanced neural regeneration and functional recovery. To analysis of neuronal morphology including soma, synapse number, and synaptic recruitment, Golgi‐cox staining was performed. Suppression of DAPK1 induced loss of dendrites length and spine density of pyramidal neurons, and supported progressive improvement of neurological deficits compared to control (P < 0.05). In addition, we investigate whether brain injury was accompanied by changes in levels of BDNF. Expression of immature precursor pro‐BDNF, involved in neuronal apoptosis, was decreased in response to ischemic injury under DAPK inhibited condition (P < 0.05). These results indicate that activation of DAPK1 following the ischemic insult exclusively correlate with brain injury and involve disturbed neurogenesis. Therefore, regulation of downstream molecules in DAPK1 pathway induces neural protection against stroke.Support or Funding InformationFunding: NRF‐2012R1A1A2005089, NRF‐2013R1A2A2A01067169
Effects of Intraperitoneal Administration of Leptin on Voluntary Feed Intake, Appetite Signaling Pathways and Metabolism in Atlantic salmon, Salmo salar
Authors: Rønnestad Ivar , Søyland Marcus AL , Hansen Tom , Jordal Ann‐Elise O , Nilsen Tom Ole , Gomes Ana S , Björnsson Björn Thrandur , Jönsson Elisabeth Bergman , Hevrøy Enst Morten 
Published: November 2023

Atlantic salmon is commercially a key species in the global aquaculture industry, and serves as a model species for teleost breeding, particularly regarding physiology and nutrition. Salmon is, however, sensitive to handling and solitary tank environment, and will respond to such stressors with reduced feed intake for extended periods. Therefore, we have validated an experimental protocol that incorporates a tank‐based system for analysis of individual feed intake in Atlantic salmon (N=16). It includes the use of sedation AQUI‐S prior to anaestesia (MS 222), allowing handling and experimental treatments like intraperitoneal (IP) injections. The protocol ensures low stress response and in the experiments described below, the salmon resumed voluntary feeding within 1–2 h of IP injections.The effects of leptin (Lep)on voluntary feed intake and appetite in post smolt Atlantic salmon was studied. Three experiments were conducted alltogether where individual salmon were placed in tanks and feed intake monitored until it stabilized at a high level, after which each individual was IP injected with recombinant salmon leptinA1 (rsLepA1) emulsified in vegetable oil. The fish were restocked into the tanks and feed intake (hand‐feeding 4 times daily) was monitored for up to 4 more days. For all experiments, fish were sampled 4 h after the last meal and samples collected from brain, liver and stomach for qPCR analysis of appetite‐ and growth‐related genes (lepa1, 2; lepr1, 2; pomca1, a2, 2s, b; agrp1, 2; cart; npy; pyy; cckl). Plasma was collected and analysed for levels of the energy‐related metabolites triglycerides, glucose, free fatty acids, lactate and D‐3‐hydroxybutyrate.Lep caused a significant reduction in feed intake for up to 3 days as well as a reduction in specific growth rate, compared to pre‐injection and sham controls. Brain expression of pomca1 and pomca2 was significantly (p<0.05) upregulated in the Lep‐treated fish. This supports earlier studies where pomc expression is linked to reduced appetite and feed intake. Brain pyy expression was significantly (p<0.05) down‐regulated in fish with reduced feed intake, sugging that PYY may be involved in the central Lep signaling pathway. Hepatic lepa1 and lepa2 mRNA expression was up‐regulated in Lep‐treated fish, but no significant differences in energy related metabolites in the plasma were found. In summary, a validated IP administration protocol for rsLepA1 has been established, demonstrating regulatory effects of homologous Lep on voluntary feed intake in Atlantic salmon.Support or Funding InformationResearch Council of Norway (grant no. 199683) and European Commission (FP7/2007‐2013; grant no 222719 – LIFECYCLE)
LIFE AND CONSCIOUSNESS AS QUALITIES
Authors: Ghosh Santibrata 
Published: November 2023

It may be presumed in this work that at the moment of death, everything in the body ( viz. molecules and their motions ) remains identical to what it was at the last moment of life, the difference being that life has something more than the basic underlying physical and chemical elements. It is a totality, which is more like a flow, (i.e. a time derivative, or differential, as in Zeno's paradox of “an arrow in flight”). This is what may be called, in a dialectical sense, a new quality that is ‘life’. A similar picture was presented about consciousness, which is a function of the central nervous system ( not the autonomic ). In both, we assumed the movement of an arrow as being at point at an instant and not there the next instant.The application of science in the hierarchy of life and consciousness is currently one of the most active areas of research in viewing the topic from the bottom‐up; i.e. chemistry >biology>neurology > consciousness. This is as opposed to a top‐down, philosophical and/or phenomenological approach to consciousness.Here we show that both ‘life’ and ‘consciousness’ belong to a category called ‘phenomenon’, both lost instantly and may also represent a new ‘quality’ in the ‘dialectical’ sense. Based on this approach, transformations in nature can be classified into the types:

A union of opposites that can generate a new quality, as in the case of an arrow in flight.
Quantity to quality; random to organized, viz. molecules to life without consciousness; is reducible.
Mechanical to dialectic with transcendental properties; life with consciousness; consciousness from neural inputs; qualitative; is irreducible.
Support or Funding Informationnone
miR‐150 regulates adipose tissue B cell function by targeting the BCR signaling pathway
Authors: Wang Haiqing , Tseng Alexander , Chang Richard Cheng‐An , Lin Yu‐lieh , Ying Wei , Zhou Beiyan 
Published: November 2023

Metainflammation and insulin resistance are two hallmarks of obesity which contribute to the pathogenesis of obesity‐associated diseases, including type 2 diabetes and cardiovascular diseases. Expansion of visceral adipose tissue (VAT) is central to the development of obesity associated metabolic syndromes, characterized by adipocyte malfunction and altered tissue specific immune cell profiles. Adipose tissue immune cells vary in number and their responses to obese stress. The adipose tissue resident B cells population dramatically expands to approximately 20% of stromal cells within obese visceral adipose tissues; however, their functions in the adipose tissue niche are poorly elucidated.Here we report that miR‐150 modulates adipose tissue function by controlling activation of B cells and their interactions with other immune cells. miR‐150KO mice displayed exacerbated obesity‐associated tissue inflammation and systemic insulin resistance, which is recapitulated by adoptive transfer of B cells, but not purified immunoglobulin, into obese Bnull mice. Using purified cell populations and a co‐culture platform, we found that miR‐150KO B cells directly enhanced proinflammatory activation of adipose tissue T cells and macrophages through cell‐cell interactions, but not through cell‐autologous mechanisms. Furthermore, miR‐150KO B cells displayed significantly enhanced antigen presentation upon stimulation, ultimately leading to elevated inflammation and insulin resistance, compared to wild type B cells. Target gene prediction analysis revealed that several targets of miR‐150, Elk1, Etf1 or Myb, are components of the B cell receptor (BCR) signaling pathway. We validated these genes as bona fide miR‐150 targets and discovered that knockdown of their expression attenuated B cell action and MHCII dependent antigen presentation. Thus, our results demonstrate a critical role for a miR‐150/BCR signaling pathway regulatory axis within adipose tissue B cells which ultimately regulate both adipose tissue metabolic and immunologic homeostasis.Support or Funding InformationAmerican Diabetes Association (1‐13‐JF‐59 to B. Zhou)National Institute of Health/National Institute of Diabetes and Digestive and Kidney Diseases (NIH/NIDDK 1R01DK098662 to B. Zhou)
Palmitoyl‐carnitine production by blood cells is associated with plasma palmitate oxidation in women
Authors: Chondronikola Maria , Asghar Rabia , Zhang Xiaojun , Dillon Edgar L , Durham William J , Wu Zhanpin , Porter Craig , Camacho‐Hughes Maria , Zhao Yingxin , Brasier Allan R , Volpi Elena , Sheffield‐Moore Melinda , Abate Nicola , Sidossis Labros , Tuvdendorj Demidmaa 
Published: November 2023

Circulating acyl‐carnitines (acyl‐CNTs) are associated with insulin resistance (IR) and type 2 diabetes (T2D) in both rodents and humans. However, the mechanisms whereby circulating acyl‐CNTs are increased in these conditions and its implications for whole‐body metabolism have not been determined. Here we aimed to determine if blood cells contribute in production of circulating acyl‐CNTs and whether such production is correlated with whole‐body fatty acid fluxes.Methods and ResultsEight non‐diabetic healthy women (Age: 47±19 y; BMI: 26±1 kg•m−2) underwent stable isotope tracer infusion and hyperinsulinemic‐euglycemic clamp study to determine in vivo whole‐body fatty acid kinetics and insulin sensitivity. At baseline (0 min) and after 3 h of hyperinsulinemic‐euglycemic clamp, blood samples were collected for measurement of in vitro synthesis rates of palmitoyl‐carnitine (palmitoyl‐CNT). The fractional synthesis rate of palmitoyl‐CNT was significantly higher during hyperinsulinemia (0.788±0.084 vs. 0.318±0.012 %•hr−1, p=0.001); however, the absolute synthesis rate did not differ between the periods (p=0.809) due to decreased (~30%) palmitoyl‐CNT concentration (p=0.189) during hyperinsulinemia. Regression analyses demonstrated that the absolute synthesis of palmitoyl‐CNT significantly correlated with the concentration of acyl‐CNTs in basal (r=0.992, p<0.001) and insulin (r=0.919, p=0.001) periods; and the basal absolute synthesis significantly correlated with plasma palmitate oxidation rate (r=0.764, p=0.027).ConclusionIn women, blood cells contribute to plasma acyl‐CNT levels and basal whole‐body plasma palmitate oxidation is associated with acyl‐CNT production. Future studies investigating the role of blood cells in acyl‐CNT and lipid metabolism under different physiological (i.e., hyperlipidemia) and pathological (i.e., IR and T2D) conditions are warranted.Support or Funding InformationClaude D. Pepper OAIC grant (# P30‐AG024832), the Institute for Translational Sciences at the UTMB, supported in part by a Clinical and Translational Science Award (#UL1 TR001439) from the NCATS/NIH, and the Shriners Grant #84090, Metabolism Unit, Shriners Hospitals for Children.
Mitogen‐Activated Protein Kinases Differentially Regulate Renal Cell Paracellular Permeability
Authors: Watari Jessica , Axis Josephine , Jaggi Shirin , Voronina Angelina , Amsler Kurt 
Published: November 2023

Movement of compounds between renal epithelial cells, paracellular permeability, is mediated primarily by the permeability of the circumferential tight junction structure (TJ) located at the apicolateral border of adjacent epithelial cells. Hydrogen peroxide (H2O2), which contributes to renal ischemia‐reperfusion injury, increased the paracellular permeability of two renal epithelial cell lines, MDCK (distal tubule) and LLC‐PK1 (proximal tubule), in a concentration‐dependent manner. H2O2 treatment also produced a concentration‐dependent increase in the phosphorylation of the Mitogen‐Activated Protein Kinases ERK 1/2, JNK 1/2, and p38MAPK. Pretreatment of renal cell populations with inhibitors of ERK 1/2 activation (U0126, PD98059) and p38MAPK activity (SB202190), diminished or completely blocked the ability of H2O2 to increase paracellular permeability. In contrast, treatment with two JNK 1/2 inhibitors, SP600125 and AS601245, did not block the ability of H2O2 to increase renal paracellular permeability. In fact, treatment with JNK 1/2 inhibitors increased paracellular permeability in a concentration‐dependent manner when added alone and augmented the increase in paracellular permeability when added prior to H2O2 treatment. Previous studies demonstrated that treatment of renal epithelial cells with H2O2 slowed the movement of GFP‐occludin into the TJ region, as measured by Fluorescence Recovery After Photobleaching. Treatment of cell populations with U0126 alone slowed the movement of GFP‐occludin into the TJ region. In U0126‐treated cell populations, however, H2O2 treatment was unable to slow further the rate of GFP‐occludin movement into the TJ region. These results indicate: 1) H2O2 treatment increases renal epithelial paracellular permeability via activation of ERK 1/2 and p38MAPK; 2) Steady state JNK 1/2 activity may promote maintenance of the paracellular permeability barrier; and 3) The ability of H2O2 to modulate the mobility of occludin into the TJ structure may be associated with its ability to increase renal cell paracellular permeability.Support or Funding InformationResearch supported by NIH grant R15 DK091749
Peripheral Apelin Inhibits Gastrointestinal Motor Functions via CCK‐dependent Pathway
Authors: SİNEN Osman , BÜLBÜL Mehmet , İzgüt‐Uysal V. Nimet 
Published: November 2023

Apelin is the endogenous ligand of the G protein‐coupled receptor APJ. The apelinergic system and APJ receptors are widely expressed in gastrointestinal (GI) tissues including stomach, small intestine and colon, suggesting that peripheral apelin may have a regulatory role in GI motor functions. It has been shown that peripheral exogenous administration of apelin increases the release of cholecystokinin (CCK), a well‐defined GI hormone that disturbs gastric emptying (GE), colon transit (CT) and small intestinal fasting motor pattern through CCK‐1 receptors expressed on vagal afferent nerves. The present study was designed to investigate (1) the effects of peripherally administered apelin on GI motor functions and (2) the contribution of CCK in apelin‐induced alterations. For measuring solid GE, rats were given a 1.6 g of preweighed pellet following an overnight fasting. Rats were euthanized 90 min after the completion of feeding and the gastric contents were recovered, dried, and weighed. To measure CT, a silicone catheter was inserted into the proximal colon and fixed with silk sutures; whereas, a strain gage transducer was implanted on the serosal surface of duodenum for recording of intestinal fasting motor pattern. The catheter and the wires of transducer were tunneled subcutaneously and secured to the neck skin. The measurements and recordings were performed after a 7‐day recovery period. For CT measurement, 1.5 ml of phenol red solution was injected through the catheter and rats were euthanized 90 min after injection. The entire colon was removed and divided into 6 equal segments. CT was calculated as the geometric center of distribution of phenol red. In control rats, GE was found 60.1 ± 3.5%; whereas, apelin‐13 administration (100 μg, ip) significantly (p<0.05) delayed the gastric emptying 31.3 ± 2.8%. The apelin‐induced delayed GE was significantly (53.3 ± 5.8%, p<0.05) accelerated by pretreatment of CCK‐1 receptor antagonist lorglumide (2.5 mg, ip) and restored to the control level. Compared with control rats (4.1 ± 0.1), apelin‐13 significantly inhibited CT (3.2 ± 0.1%, p<0.01). However, pretreatment of lorglumide significantly attenuated (4.1 ± 0.1, p<0.05) the inhibitory effect of peripheral apelin administration. The fasting‐induced duodenal phase‐III‐like contractions were remarkably disturbed following apelin‐13 administration. However, pretreatment of lorglumide abolished the apelin‐induced alterations in intestinal fasting motor pattern. These findings suggest that peripheral apelin inhibits GI motor functions and the inhibitory effects of apelin appear to be CCK‐dependent. Peripheral apelin may have a regulatory role in postprandial changes in alimentary motor functions.Support or Funding InformationThis work is funded by The Scientific and Technological Research Council of Turkey (TUBITAK). (Research Programme 1001; project number 214S349).