Mothers vigilantly guard nests after partial brood loss: a cue of nest predation risk in a paper wasp

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Seasonal acclimatization to the hot summer over 60 days in the Republic of Korea suppresses sweating sensitivity during passive heating

The main objective of this study was to determine the central mechanisms involved in suppression of thermal sweating after seasonal acclimatization (SA) during passive heating (immersing the legs in 43 °C hot water for 30 min). Testing was performed in July (before-SA) and August (after-SA) [25.2±2.2 °C, 73.9±10.3% relative humidity (RH), Cheonan (Chungnam,126° 52′N, 33.38′E), in the Republic of Korea. All experiments were carried out in an automated climatic chamber (25.0±0.5 °C and RH 60.0±3.00%). Twelve healthy men (height, 174.6±5.40 cm; weight, 65.4±5.71 kg; age, 22.7±2.90 yr) participated. The local sweat onset time was delayed in the after-SA compared to that in the before-SA (p<0.001). The local sweat rate and whole body sweat loss volume decreased in the after-SA compared to those in the before-SA (p<0.001). In addition, evaporative loss volume decreased significantly in the after-SA compared to that in the before-SA [chest, upper-back, thigh and forearm (p<0.001)]. Changes in tympanic temperature and mean body temperature were significantly lower (p<0.05) and the basal metabolic rate decreased significantly in the after-SA compared to those in the before-SA (p<0.001). These results suggest that maintenance of a lower body temperature and basal metabolic rate can occur and blunt the central sudomotor mechanisms following seasonal acclimatization, which suppresses sweating sensitivity.     

Yield loss of faba bean (Vicia faba) due to chocolate spot (Botrytis fabae) in sole and mixed cropping systems in Ethiopia

Two field experiments were conducted during 2004 and 2005 cropping seasons at Adet Agricultural Research Center, Ethiopia to assess yield losses caused by chocolate spot(Botrytis fabae) of faba bean in sole and mixed cropping systems using two cultivars. Cropping systems were sole faba bean (FB), faba bean mixed with field pea (FB: FP), barley (FB: BA) and maize (FB: MA). Mancozeb was sprayed at the rate of 2.5 kg a.i/ha at 7-, 14- and 21-day interval to generate different levels of chocolate spot disease in all the four cropping systems, and unsprayed control was also included. The treatments were arranged in a randomised complete block design (RCBD) with four replications. FB: MA mixed cropping significantly reduced disease severity and the area under disease progress curve (AUDPC) and increased faba bean grain yield. The highest faba bean grain yield among the three mixed croppings under different spray schedules was obtained from FB: MA mixed cropping in both 2004 and 2005 (2.56 and 3.74 t/ha, respectively) cropping seasons. There were highly significant yield differences (P < 0.05) among the spray intervals of mancozeb in both seasons. The highest grain yield (4.9 t/h) was recorded from the 7-day spray interval in 2005. The unsprayed faba bean had a lower grain yield (1.9 t/ha in 2004 and 2.3 t/ha in 2005) compared to the sprayed plots. The highest relative yield loss (67.5%) was calculated in 2005 from FB: FP mixed cropping in unsprayed plots. The relative yield losses in the unsprayed plots were in the range of 35.8–41.5% in 2004 and 52.6–67.5% in the 2005 cropping season. Severity and AUDPC were inversely correlated with faba bean grain yield. Significant differences were recorded in the 100-seed weight and days to maturity (DM). The unsprayed plots had shorter DM ranging from 126 to 128.5 day (except FB: MA mixed cropping) in 2004 and 122–123.9 days in 2005. In the sprayed plots DM was relatively longer than the unsprayed plots. A higher seed weight was recorded in the sole FB (56 g) and FB: MA (55 g) mixed cropping, and the lowest value of 100-seed weight was recorded from FB: FP (53 g) mixed cropping. The productivity of the mixed cropping evaluated by land equivalent ratio (LER) exceeded that of sole cropping. Faba bean grain yield was highly influenced by the severity of chocolate spot. The disease affects the DM, forcing early maturing of the plants.     

Efficacy of intercropping and harvest time modification for reducing field infestation of maize by Sitophilus zeamais Motschulsky (Coleoptera: Curculionidae)

Most management practices of Sitophilus zeamais Motschulsky, a field-to-post-harvest insect pest of cereals, have focused on post harvest control methods. This experiment was designed to investigate the potential of cropping system and modification of time of harvest to control S. zeamais. Intercropping and harvest time modification had significant (P < 0.05) effect on the number of S. zeamais emerging 42 days post-harvest. For the early harvest (15 weeks after planting (WAP)), the mean number of S. zeamais recorded from a maize monoculture (7.39) was significantly (P < 0.05) higher than the mean numbers of weevils emerging from a maize–soybean intercrop (2.31), but not significantly higher than the number recorded in maize–groundnut (3.87) intercrop. For the late harvest (18 WAP), the mean number of emerged adult observed in the maize–soybean intercrop (6.13) was significantly lower than the mean number of adult emerging from the monocrop maize (13.24). Maize–groundnut intercrop did not significantly reduce field infestation of S. zeamais compared with monocrop maize. Percentage weight loss observed in early harvested maize was significantly (P < 0.0001) lower than what was observed in late-harvested maize. Percentage weight loss was highest in stored maize harvested from monocrop maize plots for the early harvest, whereas intercropping maize with soybean reduced percentage weight loss when harvest was delayed.     

Regulation of cell proliferation and migration in gallbladder cancer by zinc finger X-chromosomal protein

Gallbladder carcinoma (GBC) is one of the mostly aggressive and fatal malignancies. However, little is known about the oncogenic genes that contributed to the development of GBC. Zinc finger X-chromosomal protein (ZFX) was a novel member of the Krueppel C2H2-type zinc-finger protein family and its down-regulation led to impaired cell growth in human laryngeal squamous cell carcinoma. Here, we aim to investigate the function of ZFX in GBC cell proliferation and migration. Loss of function analysis was performed on GBC cell line (GBC-SD) using lentivirus-mediated siRNA against ZFX. The proliferation, in vitro tumorigenesis (colony-formation) ability as well as cell migration was significantly suppressed after GBC-SD cells which were infected with ZFX-siRNA-expressing lentivirus (Lv-shZFX). Our finding suggested that ZFX promoted the growth and migration of GBC cells and could present a potential molecular target for gene therapy of GBC.     

Fibroblast Circadian Rhythms of PER2 Expression Depend on Membrane Potential and Intracellular Calcium

The suprachiasmatic nucleus (SCN) of the hypothalamus synchronizes circadian rhythms of cells and tissues throughout the body. In SCN neurons, rhythms of clock gene expression are suppressed by manipulations that hyperpolarize the plasma membrane or lower intracellular Ca²⁺. However, whether clocks in other cells also depend on membrane potential and calcium is unknown. In this study, the authors investigate the effects of membrane potential and intracellular calcium on circadian rhythms in mouse primary fibroblasts. Rhythms of clock gene expression were monitored using a PER2::LUC knockin reporter. Rhythms were lost or delayed at lower (hyperpolarizing) K⁺ concentrations. Bioluminescence imaging revealed that this loss of rhythmicity in cultures was due to loss of rhythmicity of single cells rather than loss of synchrony among cells. In lower Ca²⁺ concentrations, rhythms were advanced or had shorter periods. Buffering intracellular Ca²⁺ by the calcium chelator 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis acetoxymethyl ester (BAPTA-AM) or manipulation of inositol triphosphate (IP₃)-sensitive intracellular calcium stores by thapsigargin delayed rhythms. These results suggest that the circadian clock in fibroblasts, as in SCN neurons, is regulated by membrane potential and Ca²⁺. Changes in intracellular Ca²⁺ may mediate the effects of membrane potential observed in this study. (Author correspondence: welshdk@ucsd.edu)     

Shift Work and Inter‐Individual Differences in Sleep and Sleepiness

Inter‐individual differences in tolerance for shift work have been studied primarily in terms of external factors affecting alertness on the job or the ability to rest and sleep while at home. However, there is increasing evidence that neurobiological factors play a role as well, particularly the major processes involved in the regulation of sleep and wakefulness. These include a sleep homeostatic process seeking to balance wakefulness and sleep and a circadian process seeking to promote wakefulness during the day and sleep during the night. Shift work is associated with a temporal misalignment of these two endogenous processes. During nightwork, this misalignment makes it difficult to stay awake during the nightshift and sleep during the day. However, inter‐individual variability in the processes involved in sleep/wake regulation is substantial. Recent studies have demonstrated the existence of inter‐individual differences in vulnerability to cognitive deficits from sleep loss. Moreover, these inter‐individual differences were shown to constitute a trait. Interestingly, self‐evaluations of sleepiness did not correspond well with the trait inter‐individual variability in objective levels of performance impairment during sleep deprivation. Perhaps because of this discrepancy, in operational settings, the inter‐individual differences in vulnerability to sleep loss do not appear to be limited due to self‐selection mechanisms. Indeed, even among a highly select group of active‐duty jet fighter pilots flying a series of simulated night missions, systematic inter‐individual differences in performance impairment from sleep loss were still observed. There are significant personal and economic consequences to human error and accidents caused by performance deficits due to sleep loss. It is important, therefore, to study the inter‐individual differences in the regulation of sleep and wakefulness in the work environment so that cognitive impairment during shift work may be better anticipated and prevented.     

Facilitated Hyperpolarization Signaling in Vascular Smooth Muscle-overexpressing TRIC-A Channels

The TRIC channel subtypes, namely TRIC-A and TRIC-B, are intracellular monovalent cation-specific channels and likely mediate counterion movements to support efficient Ca²⁺ release from the sarco/endoplasmic reticulum. Vascular smooth muscle cells (VSMCs) contain both TRIC subtypes and two Ca²⁺ release mechanisms; incidental opening of ryanodine receptors (RyRs) generates local Ca²⁺ sparks to induce hyperpolarization and relaxation, whereas agonist-induced activation of inositol trisphosphate receptors produces global Ca²⁺ transients causing contraction. Tric-a knock-out mice develop hypertension due to insufficient RyR-mediated Ca²⁺ sparks in VSMCs. Here we describe transgenic mice overexpressing TRIC-A channels under the control of a smooth muscle cell-specific promoter. The transgenic mice developed congenital hypotension. In Tric-a-overexpressing VSMCs from the transgenic mice, the resting membrane potential decreased because RyR-mediated Ca²⁺ sparks were facilitated and cell surface Ca²⁺-dependent K⁺ channels were hyperactivated. Under such hyperpolarized conditions, L-type Ca²⁺ channels were inactivated, and thus, the resting intracellular Ca²⁺ levels were reduced in Tric-a-overexpressing VSMCs. Moreover, Tric-a overexpression impaired inositol trisphosphate-sensitive stores to diminish agonist-induced Ca²⁺ signaling in VSMCs. These altered features likely reduced vascular tonus leading to the hypotensive phenotype. Our Tric-a-transgenic mice together with Tric-a knock-out mice indicate that TRIC-A channel density in VSMCs is responsible for controlling basal blood pressure at the whole-animal level.     

Energetics and Location of Phosphoinositide Binding in Human Kir2.1 Channels

Kir2.1 channels are uniquely activated by phosphoinositide 4,5-bisphosphate (PI(4,5)P₂) and can be inhibited by other phosphoinositides (PIPs). Using biochemical and computational approaches, we assess PIP-channel interactions and distinguish residues that are energetically critical for binding from those that alter PIP sensitivity by shifting the open-closed equilibrium. Intriguingly, binding of each PIP is disrupted by a different subset of mutations. In silico ligand docking indicates that PIPs bind to two sites. The second minor site may correspond to the secondary anionic phospholipid site required for channel activation. However, 96–99% of PIP binding localizes to the first cluster, which corresponds to the general PI(4,5)P₂ binding location in recent Kir crystal structures. PIPs can encompass multiple orientations; each di- and triphosphorylated species binds with comparable energies and is favored over monophosphorylated PIPs. The data suggest that selective activation by PI(4,5)P₂ involves orientational specificity and that other PIPs inhibit this activation through direct competition.     

Auxiliary KChIP4a Suppresses A-type K+ Current through Endoplasmic Reticulum (ER) Retention and Promoting Closed-state Inactivation of Kv4 Channels

In the brain and heart, auxiliary Kv channel-interacting proteins (KChIPs) co-assemble with pore-forming Kv4 α-subunits to form a native K⁺ channel complex and regulate the expression and gating properties of Kv4 currents. Among the KChIP1–4 members, KChIP4a exhibits a unique N terminus that is known to suppress Kv4 function, but the underlying mechanism of Kv4 inhibition remains unknown. Using a combination of confocal imaging, surface biotinylation, and electrophysiological recordings, we identified a novel endoplasmic reticulum (ER) retention motif, consisting of six hydrophobic and aliphatic residues, 12–17 (LIVIVL), within the KChIP4a N-terminal KID, that functions to reduce surface expression of Kv4-KChIP complexes. This ER retention capacity is transferable and depends on its flanking location. In addition, adjacent to the ER retention motif, the residues 19–21 (VKL motif) directly promote closed-state inactivation of Kv4.3, thus leading to an inhibition of channel current. Taken together, our findings demonstrate that KChIP4a suppresses A-type Kv4 current via ER retention and enhancement of Kv4 closed-state inactivation.