This note is intended to serve primarily as a reference guide to users wishing to make use of the Tropical Rainfall Measuring Mission data. It covers each of the three primary rainfall instruments: the passive microwave radiometer, the precipitation radar, and the Visible and Infrared Radiometer System on board the spacecraft. Radiometric characteristics, scanning geometry, calibration procedures, and data products are described for each of these three sensors.

This paper describes the latest improvements applied to the Goddard profiling algorithm (GPROF), particularly as they apply to the Tropical Rainfall Measuring Mission (TRMM). Most of these improvements, however, are conceptual in nature and apply equally to other passive microwave sensors. The improvements were motivated by a notable overestimation of precipitation in the intertropical convergence zone. This problem was traced back to the algorithm's poor separation between convective and stratiform precipitation coupled with a poor separation between stratiform and transition regions in the a priori cloud model database. In addition to now using an improved convective-stratiform classification scheme, the new algorithm also makes use of emission and scattering indices instead of individual brightness temperatures. Brightness temperature indices have the advantage of being monotonic functions of rainfall. This, in turn, has allowed the algorithm to better define the uncertainties needed by the scheme's Bayesian inversion approach. Last, the algorithm over land has been modified primarily to better account for ambiguous classification where the scattering signature of precipitation could be confused with surface signals. All these changes have been implemented for both the TRMM Microwave Imager (TMI) and the Special Sensor Microwave Imager (SSM/I). Results from both sensors are very similar at the storm scale and for global averages. Surface rainfall products from the algorithm's operational version have been compared with conventional rainfall data over both land and oceans. Over oceans, GPROF results compare well with atoll gauge data. GPROF is biased negatively by 9% with a correlation of 0.86 for monthly 2.5Њ averages over the atolls. If only grid boxes with two or more atolls are used, the correlation increases to 0.91 but GPROF becomes positively biased by 6%. Comparisons with TRMM ground validation products from Kwajalein reveal that GPROF is negatively biased by 32%, with a correlation of 0.95 when coincident images of the TMI and Kwajalein radar are used. The absolute magnitude of rainfall measured from the Kwajalein radar, however, remains uncertain, and GPROF overestimates the rainfall by approximately 18% when compared with estimates done by a different research group. Over land, GPROF shows a positive bias of 17% and a correlation of 0.80 over monthly 5Њ grids when compared with the Global Precipitation Climatology Center (GPCC) gauge network. When compared with the precipitation radar (PR) over land, GPROF also retrieves higher rainfall amounts (20%). No vertical hydrometeor profile information is available over land. The correlation with the TRMM precipitation radar is 0.92 over monthly 5Њ grids, but GPROF is positively biased by 24% relative to the radar over oceans. Differences between TMI-and PR-derived vertical hydrometeor profiles below 2 km are consistent with this bias but become more significant with altitude. Above 8 km, the sensors disagree significantly, but the information content is low...

Dietary fish oil containing 3 highly unsaturated fatty acids has cardioprotective and anti-inflammatory effects. Prostaglandins (PGs) and thromboxanes are produced in vivo both from the 6 fatty acid arachidonic acid (AA) and the 3 fatty acid eicosapentaenoic acid (EPA). Certain beneficial effects of fish oil

Dynamin-related protein (Drp) 1 is a key regulator of mitochondrial fission and is composed of GTP-binding, Middle, insert B, and C-terminal GTPase effector (GED) domains. Drp1 associates with mitochondrial fission sites and promotes membrane constriction through its intrinsic GTPase activity. The mechanisms that regulate Drp1 activity remain poorly understood but are likely to involve reversible post-translational modifications, such as conjugation of small ubiquitin-like modifier (SUMO) proteins. Through a detailed analysis, we find that Drp1 interacts with the SUMO-conjugating enzyme Ubc9 via multiple regions and demonstrate that Drp1 is a direct target of SUMO modification by all three SUMO isoforms. While Drp1 does not harbor consensus SUMOylation sequences, our analysis identified2 clusters of lysine residues within the B domain that serve as noncanonical conjugation sites. Although initial analysis indicates that mitochondrial recruitment of ectopically expressed Drp1 in response to staurosporine is unaffected by loss of SUMOylation, we find that Drp1 SUMOylation is enhanced in the context of the K38A mutation. This dominant-negative mutant, which is deficient in GTP binding and hydrolysis, does not associate with mitochondria and prevents normal mitochondrial fission. This finding suggests that SUMOylation of Drp1 is linked to its activity cycle and is influenced by Drp1 localization.

Diabetic neuropathy is a common complication of diabetes. While multiple pathways are implicated in the pathophysiology of diabetic neuropathy, there are no specific treatments and no means to predict diabetic neuropathy onset or progression. Here, we identify gene expression signatures related to diabetic neuropathy and develop computational classification models of diabetic neuropathy progression. Microarray experiments were performed on 50 samples of human sural nerves collected during a 52-week clinical trial. A series of bioinformatics analyses identified differentially expressed genes and their networks and biological pathways potentially responsible for the progression of diabetic neuropathy. We identified 532 differentially expressed genes between patient samples with progressing or non-progressing diabetic neuropathy, and found these were functionally enriched in pathways involving inflammatory responses and lipid metabolism. A literature-derived co-citation network of the differentially expressed genes revealed gene subnetworks centred on apolipoprotein E, jun, leptin, serpin peptidase inhibitor E type 1 and peroxisome proliferator-activated receptor gamma. The differentially expressed genes were used to classify a test set of patients with regard to diabetic neuropathy progression. Ridge regression models containing 14 differentially expressed genes correctly classified the progression status of 92% of patients (P < 0.001). To our knowledge, this is the first study to identify transcriptional changes associated with diabetic neuropathy progression in human sural nerve biopsies and describe their potential utility in classifying diabetic neuropathy. Our results identifying the unique gene signature of patients with progressive diabetic neuropathy will facilitate the development of new mechanism-based diagnostics and therapies.