Lithium metal batteries (LMBs) hold the promise to pushing cell level energy densities beyond 300 Wh kg
−1
while operating at ultra-low temperatures (< −30°C). Batteries capable of both charging and discharging at these temperature extremes are highly desirable due to their inherent reduction of external warming requirements. Here we demonstrate that the local solvation structure of the electrolyte defines the charge-transfer behavior at ultra-low temperature, which is crucial for achieving high Li metal coulombic efficiency (CE) and avoiding dendritic growth. These insights were applied to Li metal full cells, where a high-loading 3.5 mAh cm
−2
sulfurized polyacrylonitrile (SPAN) cathode was paired with a one-fold excess Li metal anode. The cell retained 84 % and 76 % of its room temperature capacity when cycled at −40 and −60 °C, respectively, which presented stable performance over 50 cycles. This work provides design criteria for ultra-low temperature LMB electrolytes, and represents a defining step for the performance of low-temperature batteries.
Neonatal maternal separation alters stress-induced responses to viscerosomatic nociceptive stimuli in rat. Am J Physiol Gastrointest Liver Physiol 282: G307-G316, 2002. First published October 3, 2001 10.1152/ajpgi.00240.2001.-This study investigated the combined effect of neonatal maternal separation and acute psychological stress on pain responses in adult rats. Long-Evans dams and their male pups were reared under two conditions: 1) 180 min daily maternal separation (MS180) on postnatal days 2-14 or 2) no handling or separation (NH). At 2 mo of age, visceromotor responses to graded intensities of phasic colorectal distension (10-80 mmHg) at baseline as well as following acute 60 min water avoidance stress (WA) were significantly higher in MS180 rats. Both groups showed similar stress-induced visceral hyperalgesia in the presence of naloxone (20 mg/kg ip). MS180 rats had smaller stress-induced cutaneous analgesia in the tail-flick test compared with NH rats, with a residual naloxone-resistant component. MS180 rats showed an enhanced fecal pellet output following WA or exposure to a novel environment. These data suggest that early life events predispose adult Long-Evans rats to develop visceral hyperalgesia, reduced somatic analgesia, and increased colonic motility in response to an acute psychological stressor, mimicking the cardinal features of irritable bowel syndrome. irritable bowel syndrome; stress; analgesia; naloxone IRRITABLE BOWEL SYNDROME (IBS) is a disorder characterized by chronic abdominal pain and discomfort associated with alterations in bowel habits in the absence of a demonstrable pathology (67). Although IBS is likely a heterogeneous disorder in terms of etiology and pathophysiology, alterations in bowel habits are likely related to alterations in autonomic regulation of the gut, whereas symptoms of abdominal pain and discomfort are thought to involve additional changes in the perception of visceral events, in the form of visceral hyperalgesia or allodynia (46, 48). Additionally, in IBS patients without a concurrent diagnosis of fibromyalgia, visceral hypersensitivity is associated with a normal or diminished somatic pain sensitivity to noxious stimuli (13).Progress in the development of more effective therapies has been hampered due to the lack of animal models that mimic the key features of IBS, in particular the enhanced perception of visceral events. Many investigations have utilized acute inflammatory insults to the gut using agents such as glycerol, mustard oil, acetic acid, or zymosan to produce acute visceral hypersensitivity, thereby mimicking inflammatory bowel disorders. However, IBS is a chronic disorder characterized by the absence of inflammatory changes in the gut mucosa. More recently, several potential IBS models have been reported, all of which mimic certain aspects of the human syndrome (2, 15, 62, 72). They include an early life colon irritation model (2), an adult stress sensitization model (62), and an adult postinfection model in the rat (15) and in the mouse (72). Alt...
Thermo-electrochemical cells have potential to generate thermoelectric voltage 1 order higher than that given by semiconductor materials. To overcome the current issues in thermoelectric energy conversion, it is of paramount importance to grow and fulfill the full potential of thermo-electrochemical cells. Here we report a rational supramolecular methodology that yielded the highest Seebeck coefficient of ca. 2.0 mV K(-1) around ambient temperatures. This is based on the encapsulation of triiodide ions in α-cyclodextrin, whose equilibrium is shifted to the complexation at lower temperatures, whereas it is inverted at elevated temperatures. This temperature-dependent host-guest interaction provides a concentration gradient of redox ion pairs between two electrodes, leading to the eminent performance of the thermo-electrochemical cells. The figure of merit for this system, zT reached a high value of 5 × 10(-3). The introduction of host-guest chemistry to thermoelectric cells thus provides a new perspective in thermoelectric energy conversion.
Purpose: The expression of suppressors of cytokine signaling 1 (SOCS1) and SOCS3 genes is dysregulated in several solid tumors, causing aberrant activation of cell growth and survival signaling pathways. In this study, we analyzed SOCS1 and SOCS3 gene expression in glioblastoma multiforme (GBM) and studied the role of each protein in GBM cell signaling and radiation resistance. Experimental Design: SOCS1and SOCS3 gene expression was analyzed in 10 GBM cell lines by reverse transcription-PCR and Western blotting. SOCS3 expression was also studied in 12 primary GBM tissues by immunohistochemistry.The methylation status of the SOCS1and SOCS3 loci was determined by methylation-specific PCR. Extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinase (MAPK) activation in GBM cell lines overexpressing SOCS1 or lacking SOCS3 was determined by phosphorylated-specific Western blotting. Radiation responses in SOCS1-positive and SOCS3-deficient GBM cell lines and fibroblasts from wild-type and SOCS1or SOCS3 knockout mice were studied in a clonogenic survival assay.Results: All GBM cell lines tested lacked SOCS1expression, whereas GBM cell lines and primary GBM tumor samples constitutively expressed SOCS3. SOCS1 gene repression was linked to hypermethylation of the SOCS1genetic locus in GBM cells. Reintroduction of SOCS1or blocking SOCS3 expression sensitized cells to radiation and decreased the levels of activated ERK MAPKs in GBM cells. Conclusions: SOCS1and SOCS3 are aberrantly expressed in GBM cell lines and primary tissues. Altered SOCS gene expression leads to increased cell signaling through the ERK-MAPK pathway and may play a role in disease pathogenesis by enhancing GBM radioresistance.
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