Finally, HDR is one of the salvage treatment options for locally recurrent prostate cancer [24], [25], [26], [27] and [28]. There are currently two common

ways to perform dosimetry and treatment planning for prostate HDR brachytherapy, based on the image acquisition modality and its timing relative to the insertion of the brachytherapy catheters: CT-based and real-time TRUS based. Each method has advantages and disadvantages; choosing one or the other is a matter of departmental resources, site-specific logistics, experience, and personal preferences. TRUS-guided Talazoparib cell line HDR catheter insertion is the first of four steps using this method. The catheter insertion is performed under anesthesia in an operating or procedure room. After postoperative recovery, the patient is transferred to a CT scanner for Step 2 where simulation images are obtained find more and refinements of the catheter positions can be made. CT is most often used for this purpose because they are much more available and practical, although MRI scanners provide better anatomic detail of the prostate and surrounding anatomy. Once approved, the CT image data set is

transferred to a treatment planning computer for Step 3 where contours of the target and OARs are generated. Implant catheter distributions are registered and dose calculations are made to produce isodose clouds, dose volume histograms, and virtual dosimetry images. After dosimetry is reviewed and approved by the physician, the plan is uploaded to the treatment console, which transfers the source

delivery instructions to the robotic afterloader and where data about the final step, HDR treatment, are monitored. CT-based dosimetry offers excellent visualization of the brachytherapy catheters and OARs (rectum, urethra, and bladder) and it allows time for careful assessment of the dosimetry (Fig. 1). Although the prostate is more accurately contoured on TRUS, the CT scans can be fused with MRI to gather even more detailed information on key anatomic relationships. Except where dosimetry is performed in a room shielded for HDR brachytherapy, CT simulation in its current form often involves moving the patient. Therefore, the potential disadvantages of CT dosimetry are the need to move the patient and the time it takes to go from one location to another to perform serial functions. Moreover, changes in catheter ID-8 positions that occur between simulation and treatment delivery must be identified and corrected. This method uses the ultrasound images and computer planning in “real-time” to simultaneously guide brachytherapy catheter placement and to perform the dosimetry calculations. It has the advantages that the ultrasound clearly delineates; the prostate capsule and treatment can be delivered immediately afterward without moving the patient, if the implant procedure is performed in a properly shielded venue (i.e., a shielded operating room or brachytherapy suite).

17, 20, 21 and 22 The

study was approved by Oxfordshire Research Ethics Committee B (08/H0605/102). Nasal swabs were taken by all participants on recruitment under research nurse supervision. A dry Talazoparib purchase cotton swab was placed in the tip of both nostrils and rotated three times. All S. aureus positive participants, all students and all participants from the last practice were posted a nasal swabbing kit one and two months after recruitment, and then every two months thereafter. The swabbing technique was demonstrated on recruitment and explained in a leaflet included with each kit. Swabs were returned by post in charcoal medium (typically <1 week), and stored at 4 °C on receipt before processing (processing took <1 week; up to two weeks in total). As the study objective was to investigate S. aureus dynamics,

isolation protocols focussed on identifying all strains, even those present at low frequencies. To increase the sensitivity of culture, swabs were therefore incubated overnight at 37 °C in 5% NaCl enrichment broth (E&O Laboratories, Bonnybridge, UK). A 5 mm loop-full of broth was sub-cultured onto SASelect® chromogenic agar (Bio-Rad, Limerick, Ireland) and incubated at 37 °C overnight. Pink colonies were tested further using DNAse, catalase and Staphaurex tests following standard procedures. 23 Samples positive in all three tests were presumed to be S. aureus. A selection of pink colonies from the SASelect agar were resuspended Mirabegron in saline from which one aliquot was stored as glycerol stock at −20 °C

and another added RG7422 to 10 μl 0.85% Saline (E&O Laboratories) and 50 μl TE buffer (Sigma, Dorset, UK), heated at 99.9 °C for 10 min, then centrifuged to separate the supernatant. From this, 50 μl was removed and stored at −20 °C as a crude chromosomal DNA extract. spa-typing was performed as described, 24 with DNA amplification and sequencing using the Microlab Star Liquid Handling Workstation (Hamilton Robotics Ltd, Birmingham, UK). Chromatograms for the spa gene were assembled using Ridom StaphType. 24 Samples with mixed chromatograms were re-cultured and six-12 colonies separately typed. spa-types were grouped into spa-Clonal Complexes (CCs) using BURP clustering, and CCs labelled as their MLST equivalent for ease of comparison with other studies. 25 Epidemiological and healthcare information was collected from a structured questionnaire at recruitment, general practice and OUH records (see Supplementary Methods). After two years follow-up, general practice and OUH records were re-reviewed to ascertain antimicrobial use and inpatient admissions throughout follow-up. (1) Loss of carriage (primary outcome) Confirmed loss of carriage was defined as two consecutive negative swabs (or two consecutive swabs without the previous spa-type for analysis of spa-types (spa-level)).

Therefore the intracranial arteries are more prone to rupture. In general, the closer the dissection to the brain is, the higher probability of brain infarction is present [19]. If the dissection is more extracranial, the higher is Cabozantinib research buy the probability of the local symptoms from space occupying lesions.

Also, pain is stronger, and may even lead to syncope. This statement is true for arterial occlusive lesions of any cause—the closer the occlusion is to the brain, the more likely that infarction will develop [18]. CCAD can also be asymptomatic and discovered through routine examination. Several cases of asymptomatic or oligosymptomatic CCAD probably remain undiagnosed [17]. Recurrence rate is relatively low, mortality rate is low and functional outcome is generally good. The traditional method for visualization of CCAD is catheter angiography that may show: smooth or slightly irregular luminal narrowing (Fig. 4), Silmitasertib tapered, flame-like, occlusion, pseudoaneurysm,

intimal flap or double lumen (specific, but only in <10%) or distal branch occlusion [20] and [21]. MR images of the eccentric or circumferential periarterial rim of intramural hematoma typically show hyper intense signal on T1 and T2 weighted images [22], [23] and [24]. MR angiography has limited value, imaging the same pathomorphologic findings as angiography [3]. MR and MRA showed sensitivity (SE) of 50–100%, and Adenosine triphosphate specificity (SP) of 29–100%. Computerized tomography (CT) and CT angiography (CTA) revealed SE of 51–100%, and SP of 67–100% [25]. Doppler and duplex sonography was underrated. Although color Doppler flow imaging (CDFI) showed good results in visualization of

the dissection [26], [27], [28], [29], [30], [31], [32], [33], [34], [35] and [36], the main limitation is visualization of the intracranial dissection, which appears to be the most common site of localization. While CDFI provides visualization of the direct and some indirect findings of CCAD, TCD enables assessment of the intracranial hemodynamic and monitoring of the embolic signals [37] and [38]. The most important issue is that neurosonological evaluation enables noninvasive daily monitoring of the course of the dissection [37] and [39]. The reported sensitivity of neurovascular ultrasound for detecting spontaneous CCAD varies from 80 to 96%. It may show direct or indirect signs [36]. Direct signs are: echolucent intramural hematoma, string sign (Figs. S5 and S6 supplementary file); double lumen, or stenosis and/or occlusion of an arterial segment usually not affected by atherosclerosis (Fig. S7 supplementary file). Indirect signs are: increased or decreased pulsatility index upstream (Fig. S8 supplementary file) or downstream of the suspected lesion; more than 50% difference in blood flow velocity (BFV) compared to the unaffected side, or detection of intracranial collateral flow.

pASARM and npASARM peptides were added to ATDC5 cells and metatarsal organ cultures at concentrations BYL719 research buy of 10, 20 and 50 μM, with controls treated with a DMSO (Sigma) carrier only. In further studies, peptides were added at a final concentration of 20 μM with experiments being performed at least 3 times. Embryonic metatarsal organ cultures provide a well‐established model of endochondral bone growth [22], [23] and [24]. Metatarsal bones were cultured in a humidified atmosphere

(37 °C, 5% CO2) in 24-well plates for up to 10 days. Each culture well contained 300 μl α-minimum essential medium (MEM) supplemented with 0.2% BSA Fraction V; 1 mmol/l β-glycerophosphate (βGP); 0.05 mg/ml L-ascorbic acid phosphate; 0.05 mg/ml gentamicin and 1.25 μg/ml fungizone (Invitrogen, Paisley, UK) as previously described [22]. For the E17 bones, the medium was changed every second or third day and for the E15 bones, the medium was not changed throughout the culture period [25]. Concentrations of peptide and DMSO carrier were however added every second day. The total length of the bone through the centre of the mineralizing zone was determined using image analysis software (DS Camera Control Unit DS-L1; Nikon) every second or third

day. learn more The length of the central mineralization zone was also measured. All results are expressed as a percentage change from harvesting length which was regarded as baseline. Metatarsals were fixed in 70% ethanol, stained with eosin dye (for visualisation) and then embedded in paraffin blocks. Samples were then were scanned

with a high-resolution μCT (μCT40; Scanco Medical, Southeastern, PA) as previously described [13] and [16]. Data were acquired at 55 KeV with 6 μm cubic voxels. Three-dimensional reconstructions for bone samples were generated with the following parameters: Gauss Sigma = 4.0; Support = 2, Lower Threshold = 90 and Upper Threshold = 1000. Tissue mineral density was derived from the linear attenuation coefficient of threshold bone through precalibration of the apparatus for the acquisition voltage chosen. The PIK3C2G bone volume (BV/TV) was measured using sections encompassing the entire metatarsal on a set of 85 sections that was geometrically aligned for each sample. On day 7 of culture, 3 μCi/ml [3H]-thymidine (Amersham Biosciences, Little Chalfont, UK) was added to each metatarsal for the last 6 h of culture [22]. After washing in PBS, the unbound thymidine was extracted using 5% trichloroacetic acid (Sigma). Metatarsals were then washed in PBS before being solubilised (NCS-II tissue solubiliser, 0.5 N, Amersham) at 60 °C for 1 h. [3H]-thymidine incorporated into DNA was determined using a scintillation counter.

Kip1/p27 is up-regulated in response to anti-proliferative signals [35] and [36]. In accordance with these observations, our study also revealed an up-regulation of Kip1/p27 and Cip1/p21, and a

decrease in the levels of CDK2, CDK4, Selleckchem ERK inhibitor cyclins E1 and D1 proteins. These results provide a mechanism by which NX induces cell cycle arrest that results in a decrease in cell proliferation of liver cancer cells. MAPKs are important upstream regulators of transcription factor activation and their signaling is critical to transduction of a wide variety of extracellular stimuli into intracellular cascades, thereby controlling the cellular events such as proliferation, differentiation and apoptosis [37]. Our results demonstrated that NX treatment blocked the phosphorylation, and hence, activation of MAPKs, including ERK1/2 p38, and JNK in liver cancer cells. These findings

are similar to previous Copanlisib nmr studies where inhibition of ERK1/2, p38 and JNK by chemopreventive agents are capable of preventing skin carcinogenesis [38] and [39]. Apoptotic cell death represents a universal and exquisitely efficient suicidal pathway and an ideal way for elimination of unwanted cells; however, cancerous cells show dysregulation of this mechanism, which makes the cells virtually immortal and resistant to stress stimuli as well as therapeutic agents [40]. Therefore, the apoptotic pathway is widely studied as a potential target for cancer chemotherapy [41] and [42]. In our study, NX treatment to liver cancer cells resulted in a dose-dependent apoptotic cell death, which would contribute to NX-mediated heptaminol cell growth inhibition. In support these findings, prior studies have shown that various chemotherapeutic phytochemicals possess the ability to induce apoptosis in cancer

cells by arresting the cell cycle progression in various phases of cell division [43], [44] and [45]. Furthermore, NX treatment to liver cancer cells results in significant decrease in the levels of Bcl-2 protein along with an increase in the levels of Bax protein, thus enhancing the Bax/Bcl-2 ratio, which favors apoptosis. Increase in Bax/Bcl-2 ratio acts as a proapoptotic signal resulting in the release of cytochrome c protein from mitochondria to cytoplasm, activating the apoptosome, which further leads to auto-activation of caspase 9 and cleavage of pro-caspase 3 to its activated form caspase 3, the executioner caspase [46], [47] and [48]. Caspases are the mediators of execution mechanism of apoptosis, and their activation results in the cleavage of PARP protein, a DNA repair enzyme in the cell, and subsequent DNA degradation and apoptotic death [21]. Since, caspase 8 was not found to be activated after NX treatment in liver cancer cells, it can be deduced that NX-induced apoptosis is mediated via activation of the intrinsic pathway.

Finally, the finding that poorer performers (identified using either Immediate or Delayed breakpoint values) exhibited poorer general memory network status is in line with the suggestion that right frontal involvement in verbal memory performance in poorer performers in older age is driven by a failing LY294002 supplier memory

network. Examination of group differences on individual regions supports the hypothesis that this right frontal involvement is required to supplement change in posterior brain functioning (Davis et al., 2007 and Park and Reuter-Lorenz, 2009). Although the participants in the current study are all generally healthy older adults, who reported no serious neurodegenerative diseases Ipilimumab datasheet at interview, nor exhibited clinically relevant cerebral features

as assessed by a consultant neuroradiologist, it is possible that these performance differences indicate different (and potentially pathological) patterns of ageing; our results indicate that those with poorer splenium integrity exhibited poorer memory performance. Whereas normal healthy ageing is characterised by an anterior greater than posterior decline in callosal FA and a concomitant increase in MD (reviewed in Sullivan & Pfefferbaum, 2007), greater tissue loss in the splenium has been associated with conversion of elderly participants to dementia over a 3-year period when compared to non-converters (overall n = 328; Frederiksen et al.,

2011). Similarly, an fMRI paradigm involving the immediate (∼7.5 sec) recall of previously-presented numerical stimuli was administered to participants with Alzheimer Disease (n = 9) and healthy controls (n = 10; Starr et al., 2005). They reported increased superior frontal activation amongst the patient group compared to controls, suggesting that this compensatory activation may be present on a spectrum between normal ageing and Alzheimer Disease. Although our current sample comprises ostensibly normal healthy community-dwelling older adults, changes are thought to occur up to a decade before an eventual Meloxicam diagnosis of probable dementia. It is plausible that poorer performers could be more susceptible to a future conversion to dementia, and prospective data regarding cognitive and neurostructural change over time with the perspective of a pre-morbid baseline will be available to address this question in the future. Though our participant numbers are not small for an MRI study, they still gave us relatively little power to investigate the complex relationships between estimates of brain structure and verbal memory. Nevertheless, this is a larger study than previously published work on this topic (Duverne et al. 2009: 32 older subjects; de Chastelaine et al. 2011: 36 older subjects).

Even if one presumes a significant

enterohepatic recycling (biliary excretion of DON-GlcA to intestines) Z-VAD-FMK in vivo complete hydrolysis of the conjugate DON-GlcA by bacterial glucuronidase would occur before fecal excretion and before freezing of the fecal samples. Similar to the results obtained from the analysis of urine, traces of DON were observed in rat feces after administration of water due to the dietary DON intake. DOM-1 was not detected in the feces samples of this group, which could be explained by the higher method’s LODs and LOQs compared to DON and by only partial conversion. Following DON application, DON and DOM-1 were found in rat feces. The de-epoxidation of DON by rat gut microbes was demonstrated by Worrell et al. (1989). Furthermore, DOM-1 was determined as the major DON-metabolite in feces (Lake et al., 1987, Worrell et al., 1989 and Yoshizawa et al., U0126 solubility dmso 1983). In accordance, we observed DOM-1 amounts in feces exceeding those of DON in 5 out of 6 animals. Considerable amounts of DOM-1 (up to 78.1 nmol) were excreted even 24–48 after dosing. In the feces of rats dosed with D3G, the vast majority of the metabolites (99.5 ± 0.4%) was excreted in form of DON and DOM-1. Only traces of D3G were detected in three out of six samples 0–24 h after treatment. These

findings prove that the non-absorbed proportion of D3G is almost completely cleaved to DON and subsequently metabolized to DOM-1 in the gut. Our results are in line with in vitro Amino acid data from Berthiller et al. (2011), who showed that several intestinal bacteria have the capability to hydrolyze D3G to DON. Similarly,

Gareis et al. (1990) demonstrated that Z14G is completely cleaved during digestion, indicating that mycotoxin glucosides in general can be deconjugated in the digestive tract of mammals. We previously postulated that D3G is hydrolyzed to DON in distal parts of the intestine, since the toxin was found to be resistant to acidic conditions and several digestive enzymes (Berthiller et al., 2011). In total, we observed higher amounts of DON in rat feces after D3G treatment compared to DON treatment. As DON is mainly absorbed in the small intestine (Dänicke et al., 2004), our data lead to the assumption that D3G is hydrolyzed distal therefrom. However, detected amounts of DON in feces varied over a wide range (82–427 nmol), which impedes firm conclusions. Thus, further experiments with more specific study designs are necessary to verify this hypothesis. It should be emphasized here that the toxins were applied to the animals by gavage to ensure complete administration. These conditions are artificial, compared to the regular uptake of the compounds with feed. Further studies (e.g. with other animal species) shall take this into account, preferably delivering the compounds mixed into the diet. After DON application, the overall amount of the recovered analytes was 554 ± 64 nmol, representing 27.6 ± 3.6% of the administered dose. In urine, 14.9 ± 5.

31 Their frequency varies widely in different studies, from 3% in children to about 58% overall.15 and 24

Despite their relatively low frequency, confetti lesions may still be useful for diagnosis and they were retained as a minor feature. Their utility in adults is limited by the fact that many adults in the general population develop similar-appearing lesions as a consequence of chronic sun exposure. In such cases, the diagnosis of confetti lesions may be supported by a history of onset in the first decade of life or by asymmetric involvement of one body region over another. Dental enamel pits, previously included as a minor feature listed as “multiple, randomly distributed pits in dental RAD001 in vitro enamel” were again included as a minor feature (Fig 6). The designation was simplified to dental

enamel pits (≥3) for the entire dentition. Dental pits are much more common in TSC patients than the general population, with Mlynarczyk reporting 100% of adult TSC patients (n = 50) as having pitting compared with 7% of 250 adult control subjects.32 Because they are relatively common in the population, they are listed as a minor feature. Gingival fibromas have long been associated with TSC and were listed as a minor feature in the 1998 consensus document (Fig 7). They occur in about 20-50% of individuals with CYC202 TSC, with greater frequency in adults than children.15, 21, 33 and 34 Fibromas in TSC may also be observed on the buccal or labial mucosa and even the tongue,34 so this criterion was modified to include fibromas at other intraoral sites. (-)-p-Bromotetramisole Oxalate A stipulation was added for the presence of two or more intraoral fibromas because solitary oral fibromas may occur in the general population, particularly on the tongue or buccal mucosa along the bite line from

repeated trauma.35 and 36 Bone cysts were included in the 1998 criteria as a minor feature of TSC. Because of the lack of specificity for TSC and because the feature is rarely identified in the absence of additional TSC clinical features, a decision was made to delete “bone cysts” from the clinical diagnostic criteria. The finding of more than one retinal hamartoma was determined to be significant and specific enough to retain as a major feature (Fig 8). These lesions have similar histologic features to the tubers located in the brains of TSC patients. They are observed in 30-50% of TSC patients and it is not unusual to have multiple lesions in the same patient.37 and 38 The prevalence of retinal hamartomas in non-TSC populations is not known, but rare case reports have been made and a recent series of 3573 healthy term newborns identified only two cases of astrocytic hamartomas in that population.39 Fortunately, these lesions in TSC usually do not cause problems with vision and are a good marker for the disease, particularly in young children who might not yet have many other features.

p., Sigma–Aldrich, selleck chemical Inc.) and bipolar platinum electrodes were placed directly in derivation DII in the subcutaneous tissue. The wires were tunneled subcutaneously and exteriorized in the cervical region of the animal. ECG and HR were evaluated in unanesthetized, freely moving rats. PhKv (0.2 mL of 2.4 μM of PhKv diluted in saline) was injected intraperitoneally. After approximately 5 min, the RR, PR and QT intervals were recorded. Data are reported as mean ± SEM. Comparisons between groups were performed

by 1-way or 2-way ANOVA followed by the Turkey and Bonferroni test, respectively. One comparison between groups was analyzed using Student t test. Significance was reported as p < 0.05. Fig. 1A, B, C show representative experiments performed to investigate the effects of native PhKv on ischemia/reperfusion-induced arrhythmias in isolated rat hearts. At the onset of reperfusion, VT and/or VF were observed in hearts perfused with normal KRS (control group, Fig. 1A). Similar behavior was observed in hearts administrated with 240 nM PhKv when injected 1 min before the reperfusion (see arrow, Fig. 1B). However, in control hearts the ischemia/reperfusion arrhythmias were observed during the whole 30 min period of reperfusion, whereas perfusion with KRS containing PhKv markedly reduced the duration of arrhythmias and favored the re-establishment of the spontaneous normal sinus rhythm. Quantification

of the reperfusion arrhythmias revealed that PhKv significantly decreased the duration

of the rhythm disturbances (ASI). This effect was blocked by atropine, thereby indicating the participation Dorsomorphin nmr of muscarinic receptors on the antiarrhythmogenic effect of PhKv (Fig. 1D). We next evaluated the effect of native PhKv on reperfusion-induced arrhythmias, when injected 1 min after the beginning of Phosphatidylinositol diacylglycerol-lyase the reperfusion period (see arrow, Fig. 1C). Interestingly, under this condition PhKv partially attenuated the duration of arrhythmias, however this result was not significant (Fig. 1D). In addition, we did not observe any significant alteration in contraction force in the isolated heart preparation (data not shown). If PhKv is going to be used as a therapeutic agent, it is important to obtain large quantities of this peptide. In order to do that, we cloned the cDNA fragment that encodes the mature peptide of the PhKv into a vector to produce a recombinant PhKv containing the same amino acid sequence as the native toxin (AECAAVYERC GKGYKRCCEE RPCKCNIVMD NCTCKKFISE). As observed in Fig. 2A, immunoblotting analysis showed that recombinant PhKv can be specifically recognized by horse polyclonal antibodies directed against P. nigriventer total venom, demonstrating the similarity between the molecular weight of native and recombinant PhKv. Next, the ability of recombinant PhKv (240 nM) to protect against ischemia/reperfusion injury in isolated rat hearts was evaluated.

29 °C) using the RCP26 scenario Lenvatinib molecular weight to 2.53 °C (1.63 °C) using the RCP85 scenario (data not shown). In general, there is significant variability in seasonal warming, expressed as SST, during the current century for the different CMIP5 ensemble mean scenarios. The Mediterranean

Sea SST is projected to warm significantly in each scenario, especially in summer (2.92–0.47 °C century− 1), as seen in Figure 7b. Similarly, the AAM sub-basin is projected to warm significantly, ranging from a maximum of 1.68–0.31 °C century− 1 in summer to a minimum of 1.35–0.29 °C century− 1 in winter. Moreover, the Black Sea is also projected to warm significantly, ranging from a maximum of 2.81–0.53 °C century− 1 in summer to a minimum of 2.33–0.51 °C century− 1 in winter (data not shown). PF-562271 cost Mediterranean Sea surface variability

is affected by a combination of oceanic and atmospheric processes and displays significant regional and seasonal behaviour. AVHRR gridded annual SST data over the Mediterranean Sea indicate a range of 3.5 °C between a maximum SST of 21.2 °C over the Levantine sub-basin and a minimum SST of 17.7 °C over the LPC sub-basin. These data also indicate a seasonal SST range of 10 °C, ranging from 15.2 °C in winter, through 18.8 °C in spring and 19.8 °C in autumn, to 25 °C in summer. The Mediterranean SST is significantly warming by 0.35 °C decade− 1, with a seasonal trend variability peaking in spring at 0.38 °C decade− 1 followed by 0.32 °C decade− 1 in summer, 0.22 °C decade− 1 in autumn and 0.160 °C decade− 1 in winter. However, the Black Sea (AAM sub-basin) displays a higher (lower) warming trend of 0.51 °C decade− 1 (0.24 °C decade− 1). This Fenbendazole annual Mediterranean warming trend agrees with the previous findings of Nykjaer (2009) and Skliris et al. (2012) but runs counter to those of D’Ortenzio et al. (2000). The disagreement with D’Ortenzio et al. (2000) is probably due to the examination of different time periods. However, the annual Black Sea SST warming trend found here is less significant than the trends calculated by Belkin (2009), probably because

Belkin’s study period extends only to 2002. The spatial distribution of SST warming trends leads to significant eddies distributed over the Mediterranean Sea, indicating significant changes in the Mediterranean Sea surface circulation in the near future. The SST warming trends in the various Mediterranean sub-basins are more (less) significant than the SST warming trends in the AAM sub-basin (Black Sea). Similarly, the COV values for the SSTs of the various Mediterranean sub-basins are higher (lower) than those for the AAM sub-basin (Black Sea). At the 95% significance level, the monthly Mediterranean SST is significantly affected by atmospheric temperature (R = 98%), total cloud cover (R = − 0.81), solar radiation to the open water surface (R = 72%), net heat loss from the sea (R = − 53%), precipitation (R = − 0.53), SLP (R = − 0.43), eastward wind stress (R = − 0.