Dr Rocino has received honoraria for speaking, organising educati

Dr Rocino has received honoraria for speaking, organising educational sessions or consultancy services from Baxter, Bayer, CSL Behring, Novo Nordisk and Wyeth Lederle. Dr Fijnvandraat has received consultancy fees from Baxter. Dr Reipert is an employee of Baxter Bioscience. Dr Windyga has received research funds from Baxter, Bayer, Novo Nordisk, Wyeth, Octapharma and honoraria KU-60019 molecular weight for speaking at scientific meetings or for consultancy services from Baxter, Bayer, Octapharma, CSL Behring, Novo Nordisk, and Biovitrum. All other authors have no disclosures to make. “
“Summary.  Haemophilia A and B in one individual

may arise from co-incident inheritance of independent mutations in the F8 and F9 genes. However, this association is rare and has been studied poorly

at a genetic level. We report a male patient with abnormal bleeding and reduced factor VIII:C (26 IU dL−1) and factor IX:C (35 IU dL−1). This index case harboured a F8 c.979C>G transversion (predictive of p.Leu327Val) and a F9 c.845A>G transition (predictive of p.His282Arg) which have been previously associated with mild haemophilia A and B, respectively. Identical F8 and F9 mutations were identified in the mother CT99021 datasheet and maternal grandmother. However, an affected maternal uncle showed only the F8 c.979C>G mutation, indicating haemophilia A alone. The sister of the index case was heterozygous only for F9 c.845A>G, indicating carriership of haemophilia B alone. The non-Mendelian inheritance of F8 c.979C>G and F9 c.845A>G in this kindred is consistent with recombination between F8 and F9 and illustrates the large recombination distance between these loci. Recognition of this phenomenon was essential for accurate genetic counselling in this kindred. “
“Summary.  Circumcision is one of the most common procedures performed

in male neonates, but few published reports have described circumcision in patients with bleeding disorders. The aim of this study was to analyse outcomes of circumcision among children evaluated at our institution to determine the extent of complications and to provide guidelines for circumcision management. We searched our patient database for records of children who medchemexpress were followed up at the Mayo Clinic Comprehensive Hemophilia Center from 2000 through 2007 and who had been circumcised. We retrospectively reviewed the medical records to document complications and determine management strategies in this patient population. Of 55 children and young adults identified (median [range] age, 15 years [11 months to 21 years]), 48 patients were circumcised. Indications for circumcision were parental request (n = 45) and medical recommendation (n = 3). Twelve of 21 patients with a known bleeding disorder at the time of circumcision received factor replacement before the procedure. Three of these 21 patients had bleeding complications.

UCP2 up-regulation in liver is also found in pathologic condition

UCP2 up-regulation in liver is also found in pathologic conditions such as steatosis and obesity, where increased or perturbed fatty acid oxidation is observed.27, 29 High UCP2 expression is also found in certain tumors where it is thought that the tumor cells utilize the GSH preserving qualities of UCP2 to promote growth and reduce ROS levels. UCP2 decreases

ROS in liver through a mechanism that is not completely understood,23, 24 yet the recent report of its crystal structure is an important step in understanding the function of UCP2.30 UCP2 may serve a protective role in mitochondria by reducing ROS levels directly, lowering mitochondrial membrane potential, transporting fatty acids and fatty EGFR inhibitor drugs acid peroxides, or a combination of the above. Most important, UCP2 is markedly induced by PPARα activation in liver, specifically hepatocytes7 coincident with the induction of mitochondrial and peroxisomal enzymes involved in fatty acid β-oxidation. Based on these data, UCP2 was viewed as a potential candidate

for a Wy-14,643-induced protein that could protect from APAP toxicity. Indeed, mice lacking expression of UCP2 were not protected against APAP toxicity by Wy-14,643, whereas forced overexpression of UCP2 in the liver of wildtype mice also protected against APAP-induced toxicity in the absence of Wy-14,643. It is noteworthy, however, that sustained expression of UCP2 may selleck products in fact be deleterious, suggesting that UCP2 expression must be tightly controlled in order to maintain its salubrious qualities. Furthermore, other UCP family members, namely UCP3, may also contribute to the protection given the reduced JNK phosphorylation in Ucp2-null mice treated with WY-14,643. Moreover, it is likely that the combined activities of PPARα

targets facilitate maximal protection, and their roles specifically at the level of maintaining mitochondrial function warrant further investigation. The question arises whether UCP2 plays a role in protecting the liver against ROS under normal physiological conditions, such as during mitochondrial fatty acid β-oxidation. In general, Ucp2-null mouse livers have elevated ROS compared with wildtype mice.31 Thus, UCP2 could serve MCE as a general protector of the liver and, in particular, of the mitochondria from oxidative stress produced by normal metabolism. Under conditions of fasting, PPARα is activated by endogenous ligands, resulting in induction of peroxisome and mitochondrial fatty acid oxidation.32 Indeed, PPARα activation by starvation results in elevated mitochondrial ROS.33 This results in elevated ROS that is neutralized by the coinduced UCP2. In the case of chemically induced hepatotoxicity that results in massively elevated and lethal levels of ROS, the protective effect of UCPs are even more essential.

UCP2 up-regulation in liver is also found in pathologic condition

UCP2 up-regulation in liver is also found in pathologic conditions such as steatosis and obesity, where increased or perturbed fatty acid oxidation is observed.27, 29 High UCP2 expression is also found in certain tumors where it is thought that the tumor cells utilize the GSH preserving qualities of UCP2 to promote growth and reduce ROS levels. UCP2 decreases

ROS in liver through a mechanism that is not completely understood,23, 24 yet the recent report of its crystal structure is an important step in understanding the function of UCP2.30 UCP2 may serve a protective role in mitochondria by reducing ROS levels directly, lowering mitochondrial membrane potential, transporting fatty acids and fatty Roxadustat cost acid peroxides, or a combination of the above. Most important, UCP2 is markedly induced by PPARα activation in liver, specifically hepatocytes7 coincident with the induction of mitochondrial and peroxisomal enzymes involved in fatty acid β-oxidation. Based on these data, UCP2 was viewed as a potential candidate

for a Wy-14,643-induced protein that could protect from APAP toxicity. Indeed, mice lacking expression of UCP2 were not protected against APAP toxicity by Wy-14,643, whereas forced overexpression of UCP2 in the liver of wildtype mice also protected against APAP-induced toxicity in the absence of Wy-14,643. It is noteworthy, however, that sustained expression of UCP2 may BMS-907351 clinical trial in fact be deleterious, suggesting that UCP2 expression must be tightly controlled in order to maintain its salubrious qualities. Furthermore, other UCP family members, namely UCP3, may also contribute to the protection given the reduced JNK phosphorylation in Ucp2-null mice treated with WY-14,643. Moreover, it is likely that the combined activities of PPARα

targets facilitate maximal protection, and their roles specifically at the level of maintaining mitochondrial function warrant further investigation. The question arises whether UCP2 plays a role in protecting the liver against ROS under normal physiological conditions, such as during mitochondrial fatty acid β-oxidation. In general, Ucp2-null mouse livers have elevated ROS compared with wildtype mice.31 Thus, UCP2 could serve medchemexpress as a general protector of the liver and, in particular, of the mitochondria from oxidative stress produced by normal metabolism. Under conditions of fasting, PPARα is activated by endogenous ligands, resulting in induction of peroxisome and mitochondrial fatty acid oxidation.32 Indeed, PPARα activation by starvation results in elevated mitochondrial ROS.33 This results in elevated ROS that is neutralized by the coinduced UCP2. In the case of chemically induced hepatotoxicity that results in massively elevated and lethal levels of ROS, the protective effect of UCPs are even more essential.

Most patients suffer a severe bleeding diathesis that includes po

Most patients suffer a severe bleeding diathesis that includes postnatal umbilical cord bleeding, cutaneous bruising and haematomas, intramuscular and joint haemorrhage, postoperative haemorrhage, impaired wound healing, spontaneous abortions in early pregnancy and intracranial haemorrhage, which is the major cause

of death [40]. Typically, bleeding EPZ-6438 symptoms occur hours or days after trauma as the initially formed uncrosslinked fibrin clot is not stable. The possible diagnosis of congenital FXIII deficiency should not be delayed in any child with an unidentified bleeding disorder. Prolonged umbilical bleeding with a normal coagulation profile mandates FXIII analysis. Congenital FXIII deficiency can be caused by mutations in both FXIII genes. More than 70 causative mutations in the FXIII-A gene have been published, but only five mutations in the FXIII-B gene (see online databases www.f13-database.de, and those held by the ISTH at www.isth.org/and www.hgmd.cf.ac.uk). Most mutations code for a single amino acid exchange resulting in defective folding and instability of the mutant protein [40]. Acquired FXIII deficiency has been

reported in several conditions. FXIII A-subunit levels fall to 20–70% from decreased synthesis or consumption. Over 30 cases of severe FXIII deficiency caused by autoantibodies against FXIII-A have also been reported (∼30% in association with systemic lupus erythematosus [SLE]). These may inhibit FXIII activation or FXIIIa activity [41]. Clinical symptoms in congenital BGB324 mouse medchemexpress FXIII deficiency may be suggestive, but the diagnosis must be based on appropriate laboratory tests. Unless there is another concomitant coagulation disorder, typical coagulation screening tests are normal. Traditionally, solubility of fibrin clots in urea, acetic acid or monochloroacetic acid solution (clot solubility test)

has been used for screening. This qualitative method detects only very severe FXIII deficiency, is not standardized, and its sensitivity depends on the fibrinogen level, the clotting reagent (thrombin and/or Ca2+) and the solubilizing agent and its concentration. The detection limit varies between <0.5% and 5% FXIII activity. The high number of undiagnosed or late-diagnosed FXIII deficiencies is partly attributable to the use of this test and it is therefore no longer recommended. Diagnosis and classification of FXIII deficiencies require a quantitative functional FXIII activity assay that detects all forms of FXIII deficiency as a first-line screening test. Quantitative FXIII activity assays are based on two assay principles: (i) Measurement of ammonia released during the transglutaminase reaction and (ii) measurement of labelled amine incorporated into a protein substrate.

Most patients suffer a severe bleeding diathesis that includes po

Most patients suffer a severe bleeding diathesis that includes postnatal umbilical cord bleeding, cutaneous bruising and haematomas, intramuscular and joint haemorrhage, postoperative haemorrhage, impaired wound healing, spontaneous abortions in early pregnancy and intracranial haemorrhage, which is the major cause

of death [40]. Typically, bleeding Wnt inhibitor symptoms occur hours or days after trauma as the initially formed uncrosslinked fibrin clot is not stable. The possible diagnosis of congenital FXIII deficiency should not be delayed in any child with an unidentified bleeding disorder. Prolonged umbilical bleeding with a normal coagulation profile mandates FXIII analysis. Congenital FXIII deficiency can be caused by mutations in both FXIII genes. More than 70 causative mutations in the FXIII-A gene have been published, but only five mutations in the FXIII-B gene (see online databases www.f13-database.de, and those held by the ISTH at www.isth.org/and www.hgmd.cf.ac.uk). Most mutations code for a single amino acid exchange resulting in defective folding and instability of the mutant protein [40]. Acquired FXIII deficiency has been

reported in several conditions. FXIII A-subunit levels fall to 20–70% from decreased synthesis or consumption. Over 30 cases of severe FXIII deficiency caused by autoantibodies against FXIII-A have also been reported (∼30% in association with systemic lupus erythematosus [SLE]). These may inhibit FXIII activation or FXIIIa activity [41]. Clinical symptoms in congenital selleck chemical medchemexpress FXIII deficiency may be suggestive, but the diagnosis must be based on appropriate laboratory tests. Unless there is another concomitant coagulation disorder, typical coagulation screening tests are normal. Traditionally, solubility of fibrin clots in urea, acetic acid or monochloroacetic acid solution (clot solubility test)

has been used for screening. This qualitative method detects only very severe FXIII deficiency, is not standardized, and its sensitivity depends on the fibrinogen level, the clotting reagent (thrombin and/or Ca2+) and the solubilizing agent and its concentration. The detection limit varies between <0.5% and 5% FXIII activity. The high number of undiagnosed or late-diagnosed FXIII deficiencies is partly attributable to the use of this test and it is therefore no longer recommended. Diagnosis and classification of FXIII deficiencies require a quantitative functional FXIII activity assay that detects all forms of FXIII deficiency as a first-line screening test. Quantitative FXIII activity assays are based on two assay principles: (i) Measurement of ammonia released during the transglutaminase reaction and (ii) measurement of labelled amine incorporated into a protein substrate.

Prophylaxis was used in 399 (192%) patients with HA; such prophy

Prophylaxis was used in 399 (19.2%) patients with HA; such prophylaxis was primary (PP) in 20.3% and secondary (SP) in 75.9% of cases. Among severe HA patients, 313 (45.9%) were on prophylaxis

(22.3% on PP and 74.7% on SP). Taking into account the patients’ age, 34.7% of severe HA adults were on prophylaxis (6% PP and 92.1% SP), whereas 71.5% of severe HA paediatric patients (40.5% PP and 55.4% SP) received this www.selleckchem.com/products/PF-2341066.html kind of treatment. Established haemophilic arthropathy (EHA) was detected in 142 from 313 severe HA patients (45.3%) on prophylaxis, but only in 2.9% of patients under PP vs. 59% of patients receiving SP. There was no EHA in adult severe HA patient on PP, whereas 70.4% on SP had joint damage (P < 0.00001). Among paediatric severe HA patients, EHA was detected in 3.3% under PP and 37.8% under SP (P < 0.00001). In conclusion, our data suggest that an early initiation of prophylaxis avoids EHA in the long-term in patients with severe HA. We should emphasize the early onset RG 7204 of prophylaxis regimens. “
“This chapter contains sections titled: Introduction Epidemiology of von Willebrand disease in women

Diagnostic aspects of von Willebrand disease in women Clinical characteristics of von Willebrand disease in women Management of von Willebrand disease-related menorrhagia Obstetric aspects of von Willebrand disease Management of von Willebrand disease during pregnancy References “
“Summary.  Thirteen patients with haemophilia A took part in this study voluntarily. They underwent an aquatic training programme medchemexpress over a 9-week period (27 sessions; three sessions per week; 1 h per session). Their motor performance was assessed by the following cardio-respiratory and mechanical variables before and after the training programme: oxygen

uptake (VO2, mL min−1), relative oxygen uptake (rel VO2, mL min−1·kg−1), carbon dioxide (CO2, mL min−1), respiratory quotient (R), heart rate (bpm) and the distance covered in 12 min (the Cooper test, m). Nine patients successfully completed the intervention and measurement protocols without bleeding or other adverse events. After the proposed training programme, significant differences between the pre-test and post-test were observed. Patients’ aerobic capacity increased considerably, and their oxygen uptake improved by 51.51% (P < 0.05), while their relative oxygen uptake went up by 37.73% (P < 0.05). Their mechanical capacity also increased considerably (14.68%, P < 0.01). Our results suggest that 27 specially designed aquatic training sessions for our patients with haemophilia A had a positive effect on their motor performance and considerably improved their aerobic and mechanical capacity without causing adverse effects. "
“Haemostatic management of surgery in patients with von Willebrand disease (VWD) includes DDAVP® or von Willebrand factor (VWF)-containing concentrates.

Prophylaxis was used in 399 (192%) patients with HA; such prophy

Prophylaxis was used in 399 (19.2%) patients with HA; such prophylaxis was primary (PP) in 20.3% and secondary (SP) in 75.9% of cases. Among severe HA patients, 313 (45.9%) were on prophylaxis

(22.3% on PP and 74.7% on SP). Taking into account the patients’ age, 34.7% of severe HA adults were on prophylaxis (6% PP and 92.1% SP), whereas 71.5% of severe HA paediatric patients (40.5% PP and 55.4% SP) received this buy RGFP966 kind of treatment. Established haemophilic arthropathy (EHA) was detected in 142 from 313 severe HA patients (45.3%) on prophylaxis, but only in 2.9% of patients under PP vs. 59% of patients receiving SP. There was no EHA in adult severe HA patient on PP, whereas 70.4% on SP had joint damage (P < 0.00001). Among paediatric severe HA patients, EHA was detected in 3.3% under PP and 37.8% under SP (P < 0.00001). In conclusion, our data suggest that an early initiation of prophylaxis avoids EHA in the long-term in patients with severe HA. We should emphasize the early onset CDK activity of prophylaxis regimens. “
“This chapter contains sections titled: Introduction Epidemiology of von Willebrand disease in women

Diagnostic aspects of von Willebrand disease in women Clinical characteristics of von Willebrand disease in women Management of von Willebrand disease-related menorrhagia Obstetric aspects of von Willebrand disease Management of von Willebrand disease during pregnancy References “
“Summary.  Thirteen patients with haemophilia A took part in this study voluntarily. They underwent an aquatic training programme MCE over a 9-week period (27 sessions; three sessions per week; 1 h per session). Their motor performance was assessed by the following cardio-respiratory and mechanical variables before and after the training programme: oxygen

uptake (VO2, mL min−1), relative oxygen uptake (rel VO2, mL min−1·kg−1), carbon dioxide (CO2, mL min−1), respiratory quotient (R), heart rate (bpm) and the distance covered in 12 min (the Cooper test, m). Nine patients successfully completed the intervention and measurement protocols without bleeding or other adverse events. After the proposed training programme, significant differences between the pre-test and post-test were observed. Patients’ aerobic capacity increased considerably, and their oxygen uptake improved by 51.51% (P < 0.05), while their relative oxygen uptake went up by 37.73% (P < 0.05). Their mechanical capacity also increased considerably (14.68%, P < 0.01). Our results suggest that 27 specially designed aquatic training sessions for our patients with haemophilia A had a positive effect on their motor performance and considerably improved their aerobic and mechanical capacity without causing adverse effects. "
“Haemostatic management of surgery in patients with von Willebrand disease (VWD) includes DDAVP® or von Willebrand factor (VWF)-containing concentrates.

A further parameter, index velocity, is defined as peak thrombin

A further parameter, index velocity, is defined as peak thrombin concentration divided by the difference between lag time

and time to peak. In brief, thrombin generation assays are able to detect and describe conditions associated with enhanced or impaired coagulation. A CAT thrombin generation curve characterized by a short lag time, high peak, short time-to-peak and high ETP is indicative of a hypercoagulable state, whereas a curve indicating prolonged lag times and decreased peak heights/ETP reflects a hypocoagulable or ‘prohaemorrhagic’ state (Table 5) [14]. In patients with haemophilia, the thrombin generation assay has been shown to detect and correlate with levels of FVIII and Bortezomib concentration factor IX [15]. Importantly, in patients with severe haemophilia but no inhibitors, the thrombin generation assay was able to distinguish among clinical phenotypes, with higher ETP values being measured in patients with a mild bleeding phenotype compared with controls whose

bleeding tendency was more typical for patients with FVIII levels below 1% (Fig. 2) [16]. The major role for thrombin generation assays is expected to be in haemophilia patients with inhibitors, specifically to monitor treatment regimens with bypassing agents and to assess the coagulation profile during ITI therapy and/or high-dose FVIII replacement therapy. Bypassing agents do not restore normal pathways of haemostasis in haemophilia but, rather, they boost the generation of thrombin [17]; this is not reflected in traditional clinical coagulation assays such as prothrombin time (PT) and activated partial thromboplastin click here time [14, 17, 18]. Ongoing laboratory investigations are attempting to identify whether a correlation exists between thrombin generation assay results and the clinical MCE公司 efficacy of bypassing agents. Likewise, efforts are underway to determine whether a correlation exists between assay results and the clinical outcome of ITI therapy and/or the incidence of breakthrough bleeds and bleeding phenotype. A considerable amount of in vitro data supports the concept that anti-FVIII inhibitor activity in patients with

severe haemophilia A is variable and complex. Epitope mapping has revealed that most FVIII inhibitors have multiple rather than single epitope specificities and that inhibitor patterns differ according to FVIII source [19]. An analysis of patient plasma samples detected major inhibitors directed against C2 and another light chain epitope in about one-third (8/23) of haemophiliacs treated with plasma-derived FVIII (pdFVIII), whereas none (0/11) of the patients treated with rFVIII showed a similar pattern. The combination of anti-A2 and anti-C2 inhibitors was detected in 45% of patients treated with rFVIII and in only 17% of those treated with pdFVIII [19]. In addition, substantial in vitro data indicate a protective role for VWF on inhibitor reactivity with FVIII [20-24].

A further parameter, index velocity, is defined as peak thrombin

A further parameter, index velocity, is defined as peak thrombin concentration divided by the difference between lag time

and time to peak. In brief, thrombin generation assays are able to detect and describe conditions associated with enhanced or impaired coagulation. A CAT thrombin generation curve characterized by a short lag time, high peak, short time-to-peak and high ETP is indicative of a hypercoagulable state, whereas a curve indicating prolonged lag times and decreased peak heights/ETP reflects a hypocoagulable or ‘prohaemorrhagic’ state (Table 5) [14]. In patients with haemophilia, the thrombin generation assay has been shown to detect and correlate with levels of FVIII and RG-7388 supplier factor IX [15]. Importantly, in patients with severe haemophilia but no inhibitors, the thrombin generation assay was able to distinguish among clinical phenotypes, with higher ETP values being measured in patients with a mild bleeding phenotype compared with controls whose

bleeding tendency was more typical for patients with FVIII levels below 1% (Fig. 2) [16]. The major role for thrombin generation assays is expected to be in haemophilia patients with inhibitors, specifically to monitor treatment regimens with bypassing agents and to assess the coagulation profile during ITI therapy and/or high-dose FVIII replacement therapy. Bypassing agents do not restore normal pathways of haemostasis in haemophilia but, rather, they boost the generation of thrombin [17]; this is not reflected in traditional clinical coagulation assays such as prothrombin time (PT) and activated partial thromboplastin Doramapimod nmr time [14, 17, 18]. Ongoing laboratory investigations are attempting to identify whether a correlation exists between thrombin generation assay results and the clinical MCE公司 efficacy of bypassing agents. Likewise, efforts are underway to determine whether a correlation exists between assay results and the clinical outcome of ITI therapy and/or the incidence of breakthrough bleeds and bleeding phenotype. A considerable amount of in vitro data supports the concept that anti-FVIII inhibitor activity in patients with

severe haemophilia A is variable and complex. Epitope mapping has revealed that most FVIII inhibitors have multiple rather than single epitope specificities and that inhibitor patterns differ according to FVIII source [19]. An analysis of patient plasma samples detected major inhibitors directed against C2 and another light chain epitope in about one-third (8/23) of haemophiliacs treated with plasma-derived FVIII (pdFVIII), whereas none (0/11) of the patients treated with rFVIII showed a similar pattern. The combination of anti-A2 and anti-C2 inhibitors was detected in 45% of patients treated with rFVIII and in only 17% of those treated with pdFVIII [19]. In addition, substantial in vitro data indicate a protective role for VWF on inhibitor reactivity with FVIII [20-24].

Nighttime observations (after 1900) were made when conditions wer

Nighttime observations (after 1900) were made when conditions were less than Beaufort 2 and the research vessel was located near the deep water edge. The research vessel motored along the edge of the sandbank where water depth typically drops, sometimes sharply, from ≤10 m to≥200 m within 0.5–1.0 km. Engines were turned off and the research platform drifted passively in the northbound current along the edge of the sandbank. A hydrophone was deployed to detect any GSK2126458 nmr acoustic cues of dolphins in the area.

Deck lights, and a floodlight located on the bridge, were used to facilitate identification and observations of both the prey and the dolphins. Although disturbance of foraging behavior is possible with lights, on occasion both deck lights and generators were turned

off during a drift and night-vision goggles allowed verification and detection of foraging dolphins. Once a drift offshore began, environmental conditions including location and water depth were recorded every 20 min. When dolphins were sighted from the boat, and often right next to the boat, group size was documented and age class composition and individual identifications were made when possible. Prey species were easily identified from the surface right next to the boat or underwater near the surface. Samples were collected using a dip net for verification during an observation or occasionally flew onto the deck during a chase by the dolphins. Divers regularly entered the water with cameras or an underwater video and hydrophones to document behaviors and sounds during feeding, as this is a semihabituated community of dolphins. buy LY2606368 On occasion, usually due to dangerous jellyfish at the surface, divers did not enter the water but observed

dolphins as they continued to chase and catch fish for hours next to the boat. Table 1 lists the number of observed foraging events and their variation in depth, distance traveled, mean duration, and prey species. Between 1991 and 2004, we collected 48 observations of nocturnal feeding. Duration of the drifting medchemexpress events ranged from 10 min to over 9 h (for some all night drifts) with an average of 3:20 h:min. Actual observations of dolphins during these drifts ranged from 10 min to over 8:45 h:min, with an average of 1:49 h:min. During foraging events, water depth ranged from a mean (± SD) minimum depth of 149.4 ± 75.9 m to a mean maximum depth of 307.6 ± 63.5 m. Observable groups (defined as animals engaged in similar behavior) of dolphins ranged in number from 1 to 15 with a mean of 6.8 ± 3.8 dolphins per foraging episode (Table S1). The most common prey species observed were flying fish (Family Exocoetidae), and squid (Doryteuthis sp.), followed by needlefish (Family Belonidae) and ballyhoo/halfbeaks (Family Hemiramphidae) (Table 1). Dolphins were observed from the surface chasing and consuming flying fish. Squid were chased just below the surface often into the depths.