A major stratospheric sudden warming (SSW) event was observed in February 2018 after a 4‐year absence since the winter of 2013/2014. Based on the reanalysis data, the polar night jet changed from a very strong state to a moderate state during 12–19 January, and the moderate westerlies directly reversed to easterlies during 5–15 February. The intensified East Asian trough, Alaskan blocking, and East U.S. trough amplified the extratropical climatological wave 2, which propagated upward into the stratosphere, leading to a vortex‐splitting SSW event. Predictions of the February 2018 SSW event are explored in hindcasts initialized 0–4 weeks in advance by the Beijing Climate Center Climate System Model. Less than 20% of the 28 ensemble members predict the reversal of [U]_{60°N, 10hPa} in hindcasts initialized 3 or 4 weeks in advance if a 5‐day error is allowed, while this ratio increases to 43% in hindcasts initialized 1 week in advance. Based on the climatological occurrence of SSW events in the forecast system, the maximum deterministic predictable limit of this event is 1–2 weeks in this forecast system. The eddy heat flux and its domination by wave 2 can only be predicted within the predictable time limit. A comparison between hindcast members initialized 2 weeks in advance suggests that the extratropical troughs and blockings are responsible for the upward propagation of waves from the troposphere to the stratosphere. The predictable limit of the stratospheric circulation pattern for the February 2018 SSW, 1–2 weeks, also generalizes to other vortex split SSW events such as the January 2009 and February 1999 cases.

Using CALIPSO‐CloudSat‐Clouds and the Earth's Radiant Energy System‐Moderate Resolution Imaging Spectrometer data set, this study documents the seasonal variation of sea ice, cloud, and atmospheric properties in the Arctic (70°N–82°N) for 2007–2010. A surface‐type stratification—consisting Permanent Ocean, Land, Permanent Ice, and Transient Sea Ice—is used to investigate the influence of surface type on low‐level Arctic cloud liquid water path (LWP) seasonality. The results show significant variations in the Arctic low‐level cloud LWP by surface type linked to differences in thermodynamic state. Subdividing the Transient Ice region (seasonal sea ice zone) by melt/freeze season onset dates reveals a complex influence of sea ice variations on low cloud LWP seasonality. We find that lower tropospheric stability is the primary factor affecting the seasonality of cloud LWP. Our results suggest that variations in sea ice melt/freeze onset have a significant influence on the seasonality of low‐level cloud LWP by modulating the lower tropospheric thermal structure and not by modifying the surface evaporation rate in late spring and midsummer. We find no significant dependence of the May low‐level cloud LWP peak on the melt/freeze onset dates, whereas and September/October low‐level cloud LWP maximum shifts later in the season for earlier melt/later freeze onset regions. The Arctic low cloud LWP seasonality is controlled by several surface‐atmosphere interaction processes; the importance of each varies seasonally due to the thermodynamic properties of sea ice. Our results demonstrate that when analyzing Arctic cloud‐sea ice interactions, a seasonal perspective is critical.

While the relationship between the Arctic sea ice loss and midlatitude winter climate has been well discussed, especially on the seasonal mean scale, it remains unclear whether the Arctic sea ice condition affects the predictability of North American cold weather on the subseasonal time scale. Here we find that, in the presence of low Barents-Kara Sea (BKS) sea ice, sudden stratospheric warmings (SSWs) can favor surface cold spells over North America at the subseasonal timescale based on observations and model experiments. A persistent ridge of wave-2 pattern emerges over the Bering Sea-Gulf of Alaska several weeks after the SSW onset, with a coherent structure from the stratosphere to the surface, which, in turn, is conducive to synoptic cold air outbreaks in Canada and midwestern USA. This highlights a planetary wave pathway relating to BKS sea ice changes, by which the stratospheric polar vortex impacts the regional surface temperature on the subseasonal scale. In contrast, this mechanism does not occur with positive BKS sea ice anomaly. These findings help to improve the subseasonal predictability over North America, especially under the background of rapid change of Arctic sea ice in a warming world.

It is well established that sudden stratospheric warming (SSW) events tend to be accompanied by continental-scale, surface cold-air outbreaks (CAOs) in midlatitudes in boreal winter. However, SSW events occur at most one to two times per winter, whereas CAOs occur three to seven times over each of the North American and Eurasian continents. Using the ERA-Interim dataset for 37 winters (November–March) from 1979 to 2016, we reveal that SSW events correspond to a large-amplitude or long-lasting subset of pulse-like, anomalously strong, stratospheric mass circulation events. The anomalously strong, stratospheric mass circulation events (referred to as PULSE events) occur more than nine times in an average winter. The “displacement” versus “split” types of SSWs tend to correspond to the “wavenumber 1” versus “wavenumber 2” types of PULSEs, though the relationship between split-type SSWs and wavenumber-2-type PULSEs is weaker. Like SSW events, PULSEs also have a close relationship with CAOs. The robust relationship with CAOs still holds for the PULSE events not accompanied by SSW events. Using PULSE events, we determine that more than 70% of CAOs in the 37 winters occur in the week before and after a PULSE event, with a false alarm rate of CAO occurrence of about 25.7%. SSW events, however, are associated with only about 5.7% of CAOs, with a false alarm rate of 21.7%. Therefore, the linkage between individual continental-scale CAOs and PULSE events represents a more generalized relationship between the stratospheric circulation anomalies and surface weather. PULSE signals should also be considered as a potentially useful stratospheric indicator of the occurrence of individual CAO events.

Background: Necrotizing enterocolitis (NEC) is the most common gastrointestinal disorder in premature neonates. Possible therapeutic approaches are centered on promoting maturation of the gastrointestinal mucosal barrier. Studies have demonstrated that antenatal administration of corticosteroids can decrease NEC incidence and mortality.Methods: Pregnant rat dams were administered dexamethasone 48 h prior to delivery. The pups were subjected to an experimental NEC-like injury protocol. Ileal tissues and sera were collected and evaluated for inflammatory cytokines, gut permeability and expressions and localizations of tight junction proteins, and surfactant protein-D by immunohistochemistry/immunofluorescent staining. Intestinal epithelial cells (IEC-6) were pretreated with SP-D to examine the effect of SP-D on tight junction protein expressions when challenged with platelet-activating factor and lipopolysaccharide to model proinflammatory insults.Results: Antenatal dexamethasone reduced systemic inflammation, preserved intestinal barrier integrity, and stimulated SP-D expression on the intestinal mucosal surface in pups exposed to NEC-like injury. Pretreatment of SP-D blocked platelet-activating factor/lipopolysaccharide-induced tight junction disruption in IEC-6 cells in vitro.Conclusions: Antenatal dexamethasone preserves the development of intestinal mucosal barrier integrity and reduces incidence and morbidity from an experimental NEC-like injury model. Dexamethasone upregulation of intestinal SP-D-protective effects on tight junction proteins.Impact: Antenatal administration of dexamethasone can function in concert with intestinal surfactant protein-D to decrease systemic inflammatory responses, and protect intestinal barrier integrity in a neonatal rat model of NEC. A novel role of intestinal SP-D in preserving tight junction protein structures under inflammatory conditions. We describe the intestinal SP-D—an overlooked role of antenatal dexamethasone in neonatal NEC?