Impact of duration thresholds on Atlantic tropical cyclone counts*

Records of Atlantic basin tropical cyclones (TCs) since the late nineteenth century indicate a very large upward trend in storm frequency. This increase in documented TCs has been previously interpreted as resulting from anthropogenic climate change. However, improvements in observing and recording practices provide an alternative interpretation for these changes: recent studies suggest that the number of potentially missed TCs is sufficient to explain a large part of the recorded increase in TC counts. This study explores the influence of another factor—TC duration—on observed changes in TC frequency, using a widely used Atlantic hurricane database (HURDAT). It is found that the occurrence of short-lived storms (duration of 2 days or less) in the database has increased dramatically, from less than one per year in the late nineteenth–early twentieth century to about five per year since about 2000, while medium- to long-lived storms have increased little, if at all. Thus, the previously documented increase in total TC frequency since the late nineteenth century in the database is primarily due to an increase in very short-lived TCs. The authors also undertake a sampling study based upon the distribution of ship observations, which provides quantitative estimates of the frequency of missed TCs, focusing just on the moderate to long-lived systems with durations exceeding 2 days in the raw HURDAT. Upon adding the estimated numbers of missed TCs, the time series of moderate to long-lived Atlantic TCs show substantial multidecadal variability, but neither time series exhibits a significant trend since the late nineteenth century, with a nominal decrease in the adjusted time series. Thus, to understand the source of the century-scale increase in Atlantic TC counts in HURDAT, one must explain the relatively monotonic increase in very short-duration storms since the late nineteenth century. While it is possible that the recorded increase in short-duration TCs represents a real climate signal, the authors consider that it is more plausible that the increase arises primarily from improvements in the quantity and quality of observations, along with enhanced interpretation techniques. These have allowed National Hurricane Center forecasters to better monitor and detect initial TC formation, and thus incorporate increasing numbers of very short-lived systems into the TC database.

4-Hydroxynonenal, an endogenous aldehyde, causes pain and neurogenic inflammation through activation of the irritant receptor TRPA1

TRPA1 is an excitatory ion channel expressed by a subpopulation of primary afferent somatosensory neurons that contain substance P and calcitonin gene-related peptide. Environmental irritants such as mustard oil, allicin, and acrolein activate TRPA1, causing acute pain, neuropeptide release, and neurogenic inflammation. Genetic studies indicate that TRPA1 is also activated downstream of one or more proalgesic agents that stimulate phospholipase C signaling pathways, thereby implicating this channel in peripheral mechanisms controlling pain hypersensitivity. However, it is not known whether tissue injury also produces endogenous proalgesic factors that activate TRPA1 directly to augment inflammatory pain. Here, we report that recombinant or native TRPA1 channels are activated by 4-hydroxy-2-nonenal (HNE), an endogenous alpha,beta-unsaturated aldehyde that is produced when reactive oxygen species peroxidate membrane phospholipids in response to tissue injury, inflammation, and oxidative stress. HNE provokes release of substance P and calcitonin gene-related peptide from central (spinal cord) and peripheral (esophagus) nerve endings, resulting in neurogenic plasma protein extravasation in peripheral tissues. Moreover, injection of HNE into the rodent hind paw elicits pain-related behaviors that are inhibited by TRPA1 antagonists and absent in animals lacking functional TRPA1 channels. These findings demonstrate that HNE activates TRPA1 on nociceptive neurons to promote acute pain, neuropeptide release, and neurogenic inflammation. Our results also provide a mechanism-based rationale for developing novel analgesic or anti-inflammatory agents that target HNE production or TRPA1 activation.

Role for protease activity in visceral pain in irritable bowel syndrome

Mediators involved in the generation of symptoms in patients with irritable bowel syndrome (IBS) are poorly understood. Here we show that colonic biopsy samples from IBS patients release increased levels of proteolytic activity (arginine cleavage) compared to asymptomatic controls. This was dependent on the activation of NF-kappaB. In addition, increased proteolytic activity was measured in vivo, in colonic washes from IBS compared with control patients. Trypsin and tryptase expression and release were increased in colonic biopsies from IBS patients compared with control subjects. Biopsies from IBS patients (but not controls) released mediators that sensitized murine sensory neurons in culture. Sensitization was prevented by a serine protease inhibitor and was absent in neurons lacking functional protease-activated receptor-2 (PAR2). Supernatants from colonic biopsies of IBS patients, but not controls, also caused somatic and visceral hyperalgesia and allodynia in mice, when administered into the colon. These pronociceptive effects were inhibited by serine protease inhibitors and a PAR2 antagonist and were absent in PAR2-deficient mice. Our study establishes that proteases are released in IBS and that they can directly stimulate sensory neurons and generate hypersensitivity symptoms through the activation of PAR2.

Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome

BACKGROUND & AIMS: The mechanisms underlying abdominal pain perception in irritable bowel syndrome (IBS) are poorly understood. Intestinal mast cell infiltration may perturb nerve function leading to symptom perception. We assessed colonic mast cell infiltration, mediator release, and spatial interactions with mucosal innervation and their correlation with abdominal pain in IBS patients. METHODS: IBS patients were diagnosed according to Rome II criteria and abdominal pain quantified according to a validated questionnaire. Colonic mucosal mast cells were identified immunohistochemically and quantified with a computer-assisted counting method. Mast cell tryptase and histamine release were analyzed immunoenzymatically. Intestinal nerve to mast cell distance was assessed with electron microscopy. RESULTS: Thirty-four out of 44 IBS patients (77%) showed an increased area of mucosa occupied by mast cells as compared with controls (9.2% +/- 2.5% vs. 3.3 +/- 0.8%, respectively; P < 0.001). There was a 150% increase in the number of degranulating mast cells (4.76 +/- 3.18/field vs. 2.42 +/- 2.26/field, respectively; P = 0.026). Mucosal content of tryptase was increased in IBS and mast cells spontaneously released more tryptase (3.22 +/- 3.48 pmol/min/mg vs. 0.87 +/- 0.65 pmol/min/mg, respectively; P = 0.015) and histamine (339.7 +/- 59.0 ng/g vs. 169.3 +/- 130.6 ng/g, respectively; P = 0.015). Mast cells located within 5 microm of nerve fibers were 7.14 +/- 3.87/field vs. 2.27 +/- 1.63/field in IBS vs. controls (P < 0.001). Only mast cells in close proximity to nerves were significantly correlated with severity and frequency of abdominal pain/discomfort (P < 0.001 and P = 0.003, respectively). CONCLUSIONS: Colonic mast cell infiltration and mediator release in proximity to mucosal innervation may contribute to abdominal pain perception in IBS patients.

Simulating the interannual variability of major dust storms on Mars using variable lifting thresholds

The redistribution of a finite amount of martian surface dust during global dust storms and in the intervening periods has been modelled in a dust lifting version of the UK Mars General Circulation Model. When using a constant, uniform threshold in the model’s wind stress lifting parameterisation and assuming an unlimited supply of surface dust, multiannual simulations displayed some variability in dust lifting activity from year to year, arising from internal variability manifested in surface wind stress, but dust storms were limited in size and formed within a relatively short seasonal window. Lifting thresholds were then allowed to vary at each model gridpoint, dependent on the rates of emission or deposition of dust. This enhanced interannual variability in dust storm magnitude and timing, such that model storms covered most of the observed ranges in size and initiation date within a single multiannual simulation. Peak storm magnitude in a given year was primarily determined by the availability of surface dust at a number of key sites in the southern hemisphere. The observed global dust storm (GDS) frequency of roughly one in every 3 years was approximately reproduced, but the model failed to generate these GDSs spontaneously in the southern hemisphere, where they have typically been observed to initiate. After several years of simulation, the surface threshold field—a proxy for net change in surface dust density—showed good qualitative agreement with the observed pattern of martian surface dust cover. The model produced a net northward cross-equatorial dust mass flux, which necessitated the addition of an artificial threshold decrease rate in order to allow the continued generation of dust storms over the course of a multiannual simulation. At standard model resolution, for the southward mass flux due to cross-equatorial flushing storms to offset the northward flux due to GDSs on a timescale of ∼3 years would require an increase in the former by a factor of 3–4. Results at higher model resolution and uncertainties in dust vertical profiles mean that quasi-periodic redistribution of dust on such a timescale nevertheless appears to be a plausible explanation for the observed GDS frequency.

Rapid-onset opioids and the management of episodic pain

This is the fourth in a short series of articles that focus on what GPs should consider when monitoring and prescribing specialist-initiated palliative-care medicines. Here, the authors summarise the key issues around the use of apid onset opioids in palliative care.

Voluntary facial displays of pain increase suffering in response to nociceptive stimulation

This study demonstrates that making a standardized pain face increases negative affect in response to nociceptive stimulation, even in the absence of social feedback. This suggests that exaggerated facial displays of pain, although often socially reinforced, may also have unintended aversive consequences.

Updated empirical model of genetically-modified maize grain production practices to achieve European Union labeling thresholds

An updated empirical approach is proposed for specifying coexistence requirements for genetically modified (GM) maize (Zea mays L.) production to ensure compliance with the 0.9% labeling threshold for food and feed in the European Union. The model improves on a previously published (Gustafson et al., 2006) empirical model by adding recent data sources to supplement the original database and including the following additional cases: (i) more than one GM maize source field adjacent to the conventional or organic field, (ii) the possibility of so-called “stacked” varieties with more than one GM trait, and (iii) lower pollen shed in the non-GM receptor field. These additional factors lead to the possibility for somewhat wider combinations of isolation distance and border rows than required in the original version of the empirical model. For instance, in the very conservative case of a 1-ha square non-GM maize field surrounded on all four sides by homozygous GM maize with 12 m isolation (the effective isolation distance for a single GM field), non-GM border rows of 12 m are required to be 95% confident of gene flow less than 0.9% in the non-GM field (with adventitious presence of 0.3%). Stacked traits of higher GM mass fraction and receptor fields of lower pollen shed would require a greater number of border rows to comply with the 0.9% threshold, and an updated extension to the model is provided to quantify these effects.

Attempts to control pain prioritize attention to signals of pain: an experimental study

Clinical evidence suggests that a persistent search for solutions for chronic pain may bring along costs at the cognitive, affective, and behavioral level. Specifically, attempts to control pain may fuel hypervigilance and prioritize attention towards pain-related information. This hypothesis was investigated in an experiment with 41 healthy volunteers. Prioritization of attention towards a signal for pain was measured using an adaptation of a visual search paradigm in which participants had to search for a target presented in a varying number of colored circles. One of these colors (Conditioned Stimulus) became a signal for pain (Unconditioned Stimulus: electrocutaneous stimulus at tolerance level) using a classical conditioning procedure. Intermixed with the visual search task, participants also performed another task. In the pain-control group, participants were informed that correct and fast responses on trials of this second task would result in an avoidance of the Unconditioned Stimulus. In the comparison group, performance on the second task was not instrumental in controlling pain. Results showed that in the pain-control group, attention was more prioritized towards the Conditioned Stimulus than in the comparison group. The theoretical and clinical implications of these results are discussed.

Non-pain goal pursuit inhibits attentional bias to pain

Although dealing with pain is a vital goal to pursue, most individuals are also engaged in the pursuit of other goals. The aim of the present experiment was to investigate whether attentional bias to pain signals is inhibited when one is pursuing a concurrent salient but nonpain task goal. Attentional bias to pain signals was measured in pain-free volunteers (n=63) using a spatial cueing task with pain cues and neutral cues. The pursuit of a concurrent goal was manipulated by including additional trials in which a digit appeared at the middle of the screen. Half of the participants (goal group) were instructed to name these additional stimuli aloud. In order to increase the affective-motivational value of this non-pain-related goal, monetary reward and punishment were made contingent upon the performance of this task. Participants of the control group did not perform the additional task. As predicted, the results show attentional bias to pain signals in the control group, but not in the goal group. This indicates that attentional bias to signals of impending pain is inhibited when one is engaged in the pursuit of another salient but nonpain goal. The results of this study underscore a motivational view on attention to pain, in which the pursuit of multiple goals, including nonpain goals, is taken into account.