Detection of recent changes in climate using meteorological data from south-eastern Bangladesh

Analysis of meteorological records from four stations (Chittagong, Cox’s Bazar, Rangamati, Sitakunda) in south-eastern Bangladesh show coherent changes in climate over the past three decades. Mean maximum daily temperatures have increased between 1980 and 2013 by ca. 0.4 to 0.6°C per decade, with changes of comparable magnitude in individual seasons. The increase in mean maximum daily temperature is associated with decreased cloud cover and wind speed, particularly in the pre- and post-monsoon seasons. During these two seasons, the correlation between changes in maximum temperature and clouds is between -0.5 and -0.7; the correlation with wind speed is weaker although similar values are obtained in some seasons. Changes in mean daily minimum (and hence mean) temperature differ between the northern and southern part of the basin: northern stations show a decrease in mean daily minimum temperature during the post-monsoon season of between 0.2 and 0.5°C per decade while southern stations show an increase of ca. 0.1 to 0.4°C per decade during the pre-monsoon and monsoon seasons. In contrast to the significant changes in temperature, there is no trend in mean or total precipitation at any station. However, there is a significant increase in the number of rain days at the northern sites during the monsoon season, with an increase per decade of 3 days in Sitakunda and 7 days at Rangamati. These climate changes could have a significant impact on the hydrology of the Halda Basin, which supplies water to Chittagong and is the major pisciculture centre in Bangladesh.

CLEC-2 is not required for platelet aggregation at arteriolar shear

The C-type lectin receptor CLEC-2 is expressed primarily on the surface of platelets, where it is present as a dimer, and is found at low level on a subpopulation of other hematopoietic cells, including mouse neutrophils [1–4] Clustering of CLEC-2 by the snake venom toxin rhodocytin, specific antibodies or its endogenous ligand, podoplanin, elicits powerful activation of platelets through a pathway that is similar to that used by the collagen receptor glycoprotein VI (GPVI) [4–6]. The cytosolic tail of CLEC-2 contains a conserved YxxL sequence preceded by three upstream acidic amino acid residues, which together form a novel motif known as a hemITAM. Ligand engagement induces tyrosine phosphorylation of the hemITAM sequence providing docking sites for the tandem-SH2 domains of the tyrosine kinase Syk across a CLEC-2 receptor dimer [3]. Tyrosine phosphorylation of Syk by Src family kinases and through autophosphorylation leads to stimulation of a downstream signaling cascade that culminates in activation of phospholipase C γ2 (PLCγ2) [4,6]. Recently, CLEC-2 has been proposed to play a major role in supporting activation of platelets at arteriolar rates of flow [1]. Injection of a CLEC-2 antibody into mice causes a sustained depletion of the C-type lectin receptor from the platelet surface [1]. The CLEC-2-depleted platelets were unresponsive to rhodocytin but underwent normal aggregation and secretion responses after stimulation of other platelet receptors, including GPVI [1]. In contrast, there was a marked decrease in aggregate formation relative to controls when CLEC-2-depleted blood was flowed at arteriolar rates of shear over collagen (1000 s−1 and 1700 s−1) [1]. Furthermore, antibody treatment significantly increased tail bleeding times and mice were unable to occlude their vessels after ferric chloride injury [1]. These data provide evidence for a critical role for CLEC-2 in supporting platelet aggregation at arteriolar rates of flow. The underlying mechanism is unclear as platelets do not express podoplanin, the only known endogenous ligand of CLEC-2. In the present study, we have investigated the role of CLEC-2 in platelet aggregation and thrombus formation using platelets from a novel mutant mouse model that lacks functional CLEC-2.