ASF) or C57BL/6 specific pathogen free mice (B6.SPF) with H. felis. After 24 weeks, both groups progressed to gastric dysplasia, but B6.SPF mice displayed decreased H. felis colonisation and acquisition of multiple new bacterial species. Potential mechanisms responsible for the ineffective H. felis clearance in the B6.ASF model Kinase Inhibitor Library solubility dmso include the absence of new gastric microbiota, the lack of expression of new gastric mucins, and a reduced ratio of H. felis–specific IgG2c:IgG1 serum antibodies. Zhang et al. [42] reported that the administration

of Lactobacillus salivarius REN to F344 rats counteracts the unfavorable 4-nitroquinoline-1-oxide-induced changes in colonic microbiota by its suppressive effect on Helicobacter spp. On the contrary, Whary et al. [43] observed that the development of typhlocolitis in H. hepaticus-infected B6.129P2-IL-10tm/Cgn (IL-10−/−) mice required co-colonisation with L. reuteri. These data contrast with previous reports by the same group showing that intestinal lesions are attenuated in H. hepaticus/L. reuteri 6798 or H. hepaticus/L. paracasei coinfected SPF B6.129 IL-10−/−

mice. However, Büchler et al. [44] selleck products revealed that strain-specific enterocolitis susceptibility in IL-10−/− mice depends on a complex interplay between host genetics and gut microbiota composition. The authors claimed that single pathogens (i.e., H. hepaticus) are not sufficient to determine whether IBD susceptibility or resistance is fully displayed. A new species-specific qPCR assay based on cdtB (cytolethal distending toxin B) was developed to detect H. pullorum in tissue and feces of infected mice [36]. A molecular enrichment strategy based on class specific amplification of the cpn10-cpn60 operon was developed for the detection of Epsilon-proteobacteria in the dog fecal microbiome, allowing the amplification of two possible novel Helicobacter spp. [45]. A combined agar and broth dilution method was developed to determinate

the antimicrobial susceptibility of H. suis [46]. selleck kinase inhibitor Finally, a review describing laboratory procedures for culture and maintenance of Helicobacter spp. was published last year [47]. Over the last year, significant advances have been made in the understanding of the biology of NHPH species, their interaction with the host, the molecular basis of transmission to humans and their potential pathogenicity for both humans and animals. Conflict of Interest: the authors have declared no conflict of interest;][#,63]?> “
“Outer inflammatory protein A (OipA) has an important role in Helicobacter pylori pathogenesis. In this study, we purified the outer membrane protein and evaluated the effects of this protein on maturation and cytokine production by dendritic cells (DCs). The oipA gene was inserted into pET28a, and this construct was transformed into Escherichia coli BL21 (DE3). Purification of the recombinant protein was performed by Ni-NTA affinity chromatography.

6-log10 IU/mL was achieved. Although end-of-treatment (EOT) HBV-DNA in four (1 8%) LMV-treated women remained at >107 IU/mL (±0.5 log IU/ml), no mother-to-baby transmission was observed. One baby from the untreated maternal group was HBsAg-positive at 9 months post-partum. Drug resistance testing compared population-based (20% quasispecies sensitivity) to ultra-deep pyrosequencing SRT1720 research buy (UDPS) (< 1 % quasispecies sensitivity). UDPS revealed that LMV therapy resulted in increased viral quasispecies diversity and the positive selection of HBV-variants with reverse transcriptase amino acid substitutions at sites associated

with primary LMV resistance (rtM204I/V and rtA1 81T) in four (19%) women. These viral variants were detected mostly at low frequencies

(0.63% to 5.92%) at EOT, but one LMV-treated mother had an rtA1 81T-variant that increased from 2.2% pre-therapy to 25.59% at EOT. This mother was also infected with the vaccine-escape variant (sG145R) which was inhibited by LMV treatment. Conclusion: LMV-therapy during late pregnancy only reduced maternal viremia moderately, and drug-resistant viral variants emerged. Disclosures: Miriam Levy – Grant/Research Support: Gilead Stephen Locarnini – Consulting: Gilead, Bristol-Myers Squibb, Merck Sharpe and Dohme; Employment: Melbourne Health The following people have nothing to disclose: Lilly Yuen, Anna Ayres, Kathy Jackson, Julianne Bayliss, Suthaharan Manoharan, Anne selleck L. Glass, Michael Maley, Scott Bowden, Fabio Luciani Background and Aims: The effectiveness Daporinad of interferon-α (IFN-α) to chronic hepatitis B has been demonstrated by many large clinical trials and meta-analyses. However, the effect of IFN-α therapy is unsatisfactory because HBV infection was considered to attenuate IFN responses in HBV-infected hepatocytes. To evaluate the improvement

of the effectiveness of IFN therapy by prior treatment with nucleot(s)ide analogues, we measured the biological markers for Th1/2 immune response in patients who underwent the sequential therapy; lamivudine (LMV) alone for 20 weeks followed by the LMV and IFN-α combination for 4 weeks and lastly IFN-α alone for 20 weeks. Then the associations between Th 1 /2 ratio and therapeutic response were evaluated. Patients and Methods: Thirty HBe antigen (HBeAg)-positive chronic hepatitis B patients who underwent sequential therapy were enrolled. Twenty four weeks after the termination of IFN treatment, the effects of the therapy were assessed by ALT normalization, HBeAg negativity, and decrease of HBV-DNA to less than 3.7 LGE/ml. Fulfillment in all three of the criteria was defined as sustained virological response (SVR), and fulfillment in two of them, ALT normalization and HBeAg negativity, as partial response (PR).

One study showed a significant improvement in reflux disease-related quality of life scores one year after H. pylori eradication therapy [10]. In another study from the United States, 1611 cases of an African–American population with esophagitis and/or gastritis and confirmed H. pylori buy BVD-523 status were included between 2004 and 2007 and compared with controls [11]. The prevalence of H. pylori in gastritis patients was 40%, in esophagitis patients 4%, and in normal controls 34%. After adjusting for age and gender, the odds ratio of H. pylori infection in the esophagitis group versus the normal group was 0.06 (95% CI 0.01−0.59; p = .01). They concluded that H. pylori has

a significant negative association with esophagitis in African–Americans, which may point to a protective role of H. pylori in the pathogenesis of esophagitis. In addition, another study on 2442 patients referred for upper gastrointestinal endoscopy observed H. pylori infection in 82% of GERD patients. A statistically significant relationship was found between H. pylori positivity and the grade of GERD [12]. In line with these observations, the updated Maastricht consensus on management of H. pylori infection concluded that H. pylori status has no effect on symptom severity, symptom recurrence, and treatment efficacy in GERD [7]. H. pylori eradication does not exacerbate pre-existing GERD nor

affect treatment efficacy. Therefore, the presence see more Erastin nmr of GERD should not dissuade to prescribe an H. pylori eradication treatment when otherwise indicated. Furthermore, long-term efficacy of PPI maintenance treatment for GERD is not influenced by H. pylori status [13]. Functional dyspepsia (FD) is currently

defined as symptoms of epigastric pain, epigastric burning, postprandial fullness, or early satiation, in the absence of any organic, systemic, or metabolic disease that is more likely to explain the symptoms [14]. This chronic, relapsing and remitting disorder is commonly seen in individuals from all around the world. Data from a large population-based study demonstrated no effect on life expectancy and no differences in the numbers of gastrointestinal related deaths between subjects with or without dyspepsia [15]. The exact role of H. pylori in FD is still under debate. Some investigators have argued that if H. pylori gastritis is considered an organic disease, H. pylori-associated FD should not be considered as a functional disorder [16, 17]. Possible mechanisms by which H. pylori may elicit dyspeptic symptoms include alterations of gastric motility, as well as endocrine and acid-secretory abnormalities [18]. Hunger sensations, acid secretion and gastrointestinal motility are regulated by ghrelin, particularly produced by the gastric enteroendocrine cell compartment [18]. Gastric infection with H. pylori is associated with decreased ghrelin secretion [19].

One study showed a significant improvement in reflux disease-related quality of life scores one year after H. pylori eradication therapy [10]. In another study from the United States, 1611 cases of an African–American population with esophagitis and/or gastritis and confirmed H. pylori http://www.selleckchem.com/products/torin-1.html status were included between 2004 and 2007 and compared with controls [11]. The prevalence of H. pylori in gastritis patients was 40%, in esophagitis patients 4%, and in normal controls 34%. After adjusting for age and gender, the odds ratio of H. pylori infection in the esophagitis group versus the normal group was 0.06 (95% CI 0.01−0.59; p = .01). They concluded that H. pylori has

a significant negative association with esophagitis in African–Americans, which may point to a protective role of H. pylori in the pathogenesis of esophagitis. In addition, another study on 2442 patients referred for upper gastrointestinal endoscopy observed H. pylori infection in 82% of GERD patients. A statistically significant relationship was found between H. pylori positivity and the grade of GERD [12]. In line with these observations, the updated Maastricht consensus on management of H. pylori infection concluded that H. pylori status has no effect on symptom severity, symptom recurrence, and treatment efficacy in GERD [7]. H. pylori eradication does not exacerbate pre-existing GERD nor

affect treatment efficacy. Therefore, the presence selleck products check details of GERD should not dissuade to prescribe an H. pylori eradication treatment when otherwise indicated. Furthermore, long-term efficacy of PPI maintenance treatment for GERD is not influenced by H. pylori status [13]. Functional dyspepsia (FD) is currently

defined as symptoms of epigastric pain, epigastric burning, postprandial fullness, or early satiation, in the absence of any organic, systemic, or metabolic disease that is more likely to explain the symptoms [14]. This chronic, relapsing and remitting disorder is commonly seen in individuals from all around the world. Data from a large population-based study demonstrated no effect on life expectancy and no differences in the numbers of gastrointestinal related deaths between subjects with or without dyspepsia [15]. The exact role of H. pylori in FD is still under debate. Some investigators have argued that if H. pylori gastritis is considered an organic disease, H. pylori-associated FD should not be considered as a functional disorder [16, 17]. Possible mechanisms by which H. pylori may elicit dyspeptic symptoms include alterations of gastric motility, as well as endocrine and acid-secretory abnormalities [18]. Hunger sensations, acid secretion and gastrointestinal motility are regulated by ghrelin, particularly produced by the gastric enteroendocrine cell compartment [18]. Gastric infection with H. pylori is associated with decreased ghrelin secretion [19].

95; 95% CI = 2.1-20.0, P < .001). The number of MTHFR 677T alleles was the best genetic predictor of Hcy levels (r2 = 0.06; P = 6.2e-6; corrected for genetic variants analyzed) and this effect remained significant after correction for other confounding factors. Using multi-dimensionality reduction XL184 order approaches, we observed significant epigenetic interaction among some of the folate-related genetic variants to predict higher Hcy levels, and also among higher Hcy levels and folate-related genetic variants to predict the end-diagnosis of MA only among migraineurs. In controls, Hcy levels and the number of MTHFR 677T alleles were found to be intermediate between those observed in MA and MO patients. Conclusion.—

Our results suggest that MA patients have higher Hcy levels. We also observed complex epigenetic interaction among folate-related enzymes, sex, and Hcy levels predicting MA phenotype. Nevertheless, genetic factors explained

only a minor proportion of the variance for both Hcy plasma levels and for predicting MA phenotype. Determination of MTHFR C677T polymorphisms and Hcy levels may be useful to identify patients with a high risk of suffering from MA. “
“In a recent Opinion Editorial posted on the Listserv of the Southern Headache Society (http://www.SouthernHeadache.org), Dr. Lawrence Robbins of the Robbins Headache FK506 price Clinic, Northbrook, Illinois, explored how headaches resulting from trauma are sometimes difficult to treat and often remain refractory. Most neurologists likely encounter young athletes who have a moderate-to-severe post-concussion syndrome. The following discussion, therefore, is relevant to the practice of headache medicine. In this Point Counterpoint, Dr. Robbins has repurposed his OpEd once more for Headache, followed by a response from Dr. Frank Conidi of the Florida Center for Headache and Sports Neurology, and Team Neurologist for the Florida Panthers

of the National Hockey League. The discussion concludes with a retort from Dr. Robbins. “
“(Headache 2011;51:985-991) Objectives.— This study provides preliminary data and a framework to facilitate cost comparisons see more for pharmacologic vs behavioral approaches to headache prophylactic treatment. Background.— There are few empirical demonstrations of cumulative costs for pharmacologic and behavioral headache treatments, and there are no direct comparisons of short- and long-range (5-year) costs for pharmacologic vs behavioral headache treatments. Methods.— Two separate pilot surveys were distributed to a convenience sample of behavioral specialists and physicians identified from the membership of the American Headache Society. Costs of prototypical regimens for preventive pharmacologic treatment (PPT), clinic-based behavioral treatment (CBBT), minimal contact behavioral treatment (MCBT), and group behavioral treatment were assessed.

95; 95% CI = 2.1-20.0, P < .001). The number of MTHFR 677T alleles was the best genetic predictor of Hcy levels (r2 = 0.06; P = 6.2e-6; corrected for genetic variants analyzed) and this effect remained significant after correction for other confounding factors. Using multi-dimensionality reduction LBH589 ic50 approaches, we observed significant epigenetic interaction among some of the folate-related genetic variants to predict higher Hcy levels, and also among higher Hcy levels and folate-related genetic variants to predict the end-diagnosis of MA only among migraineurs. In controls, Hcy levels and the number of MTHFR 677T alleles were found to be intermediate between those observed in MA and MO patients. Conclusion.—

Our results suggest that MA patients have higher Hcy levels. We also observed complex epigenetic interaction among folate-related enzymes, sex, and Hcy levels predicting MA phenotype. Nevertheless, genetic factors explained

only a minor proportion of the variance for both Hcy plasma levels and for predicting MA phenotype. Determination of MTHFR C677T polymorphisms and Hcy levels may be useful to identify patients with a high risk of suffering from MA. “
“In a recent Opinion Editorial posted on the Listserv of the Southern Headache Society (http://www.SouthernHeadache.org), Dr. Lawrence Robbins of the Robbins Headache PD0325901 research buy Clinic, Northbrook, Illinois, explored how headaches resulting from trauma are sometimes difficult to treat and often remain refractory. Most neurologists likely encounter young athletes who have a moderate-to-severe post-concussion syndrome. The following discussion, therefore, is relevant to the practice of headache medicine. In this Point Counterpoint, Dr. Robbins has repurposed his OpEd once more for Headache, followed by a response from Dr. Frank Conidi of the Florida Center for Headache and Sports Neurology, and Team Neurologist for the Florida Panthers

of the National Hockey League. The discussion concludes with a retort from Dr. Robbins. “
“(Headache 2011;51:985-991) Objectives.— This study provides preliminary data and a framework to facilitate cost comparisons check details for pharmacologic vs behavioral approaches to headache prophylactic treatment. Background.— There are few empirical demonstrations of cumulative costs for pharmacologic and behavioral headache treatments, and there are no direct comparisons of short- and long-range (5-year) costs for pharmacologic vs behavioral headache treatments. Methods.— Two separate pilot surveys were distributed to a convenience sample of behavioral specialists and physicians identified from the membership of the American Headache Society. Costs of prototypical regimens for preventive pharmacologic treatment (PPT), clinic-based behavioral treatment (CBBT), minimal contact behavioral treatment (MCBT), and group behavioral treatment were assessed.

3B,C). This antimitotic effect of HDAC6

could be partially explained by the disruption of cell growth regulation. Thus, we next examined the effect of HDAC6 on the cell cycle distribution and on the apoptosis of Hep3B cells. Flow cytometry of Annexin V-stained cells showed no significant induction of apoptosis versus control (non- or empty vector-transfected) cells (Fig. 3D). In addition, HDAC6 overexpression did not affect www.selleckchem.com/products/AG-014699.html the expressions of proapoptotic molecules, such as apoptosis-inducing factor (AIF), Bax, or Apaf-1 (data not shown), nor did it cause caspase-3 or poly (ADP-ribose) polymerase (PARP) cleavage of Hep3B cells (Fig. 3E). Moreover, when propidium iodide-stained HDAC6 transfected cells were performed using flow cytometry, no significant changes in cell cycle transition were observed versus control cells (Supporting Fig. 2). Likewise, the ectopic overexpression of HDAC6 did not affect the expressions of cell cycle proteins such as p15INK4B, p21WAF1/Cip1, or cyclin-dependent kinase 2 (CDK2) (Fig. 3F). These results suggest that HDAC6 overexpression induces a mitotic defect possibly mediated by caspase-independent cell death. It has been well established that autophagy is an evolutionarily conserved protein degradation process, which plays essential roles in cell survival or cell death, depending on the cellular context.

The fact that HDAC6, a ubiquitin-binding deacetylase, Forskolin is a central component of basal autophagy that targets protein aggregates and damages mitochondria10 led selleck screening library us to investigate whether the ectopic expression of HDAC6 elicits autophagic cell death of HCC cells. Notably, it was found that ectopic expression of HDAC6 in Hep3B cells significantly increased the conversion of LC3B-I into LC3B-II (Fig. 4A,B), whereas treatment of 3-methyladenine (3-MA; a specific inhibitor of autophagy) effectively blocked LC3B-II conversion induced by HDAC6 in Hep3B cells (Fig. 4C). Consistently, reduced cell viability caused by ectopic HDAC6 expression was effectively

blocked by 3-MA treatment (Fig. 4D). In addition, immunofluorescence staining for LC3B revealed that HDAC6 overexpression induced ring-shaped spots evenly distributed throughout cytoplasm, indicating an association between LC3 and autophagosomal membranes, and this association was completely blocked by 3-MA (Fig. 4E). Moreover, when cells were treated with HDAC6-sepcific inhibitors (Tubastatin A [Tub A] and Tubacin), ectopic overexpression of HDAC6 did not elicit hypoacetylation of α-tubulin, nor did it cause LC3B-II conversion in Hep3B cells (Fig. 4F). These results suggest that the restoration of HDAC6 expression activates autophagic cell death and the functional deacetylase activity of HDAC6 is required for the autophagy activation in hepatocarcinogenesis.

Along with the histological findings, the

mRNA expression level of AQP4 in the stomach of the H2R knockout mouse was significantly higher than that of wild type regardless of the aging period (Fig. 2a). However, the mRNA expression level of AQP4 in 60 weeks old was significantly lower than those in 20 weeks old. The mRNA expression level of H+/K+-ATPase in the stomach of the H2R knockout mouse was higher than that of wild type at the age of 20 weeks and 40 weeks (Fig. 2b). However, it was gradually decreased through the aging in the H2R knockout mouse. In addition, the ratio HDAC activation of the mRNA expression between AQP4 and H+/K+-ATPase were higher in the H2R knockout mouse regardless of the aging period compared with wild type (Fig. 2c). To summarize these data, the mucosal hyperplasia was induced in the H2R knockout mouse and was aggravated by aging along with the decrease of the mRNA expression of H+/K+-ATPase. The mRNA expression of AQP4 was significantly higher in the H2R knockout mouse but was decreased by aging. The higher ratio of mRNA expression between AQP4 and H+/K+-ATPase was kept

in the H2R knockout mouse, suggesting that the decrease of AQP4 mRNA levels by aging was caused by reduced viability of gastric parietal cells. Subsequently, the influence on H. pylori infection for the gastric mucosal status of SPEM was assessed in wild type or the H2R knockout mice. In the wild type mice, the mRNA expression level of Shh, which is a morphogen for differentiation of gastric mucosal cells, in the stomach was significantly decreased by H. pylori infection (Fig. 3a). Nutlin-3 molecular weight In the H2R knockout mouse, the mRNA expression level of Shh

was lower than that of wild type. The mRNA expression this website level of Shh was the lowest in the H2R knockout mouse with H. pylori infection. The mRNA level of TFF2, which is an indicator of SPEM, was significantly higher in the H2R knockout mouse compared with that of wild type (Fig. 3b). Furthermore, it was increased by H. pylori infection in the wild type and in the H2R knockout mouse. These data suggest that SPEM in the H2R knockout mouse with H. pylori infection would be the most severe among these mice. The fluorescent immunochemistry of AQP4 and H+/K+-ATPase was performed using these mice. In the wild type mice, the infection of H. pylori decreased the expression of AQP4 in the stomach (Fig. 4). Similarly, in the H2R knockout mouse, the infection of H. pylori suppressed the expression of AQP4 as compared with that without the infection of H. pylori, while mucosal hyperplasia with multiple cystic dilatations was observed regardless of the infection of H. pylori. The mRNA expression of AQP4 was significantly decreased by infection of H. pylori in the wild type as well as in the H2R knockout mouse (Fig. 5a). The mRNA expression level of H+/K+-ATPase was also decreased by infection of H.

Along with the histological findings, the

mRNA expression level of AQP4 in the stomach of the H2R knockout mouse was significantly higher than that of wild type regardless of the aging period (Fig. 2a). However, the mRNA expression level of AQP4 in 60 weeks old was significantly lower than those in 20 weeks old. The mRNA expression level of H+/K+-ATPase in the stomach of the H2R knockout mouse was higher than that of wild type at the age of 20 weeks and 40 weeks (Fig. 2b). However, it was gradually decreased through the aging in the H2R knockout mouse. In addition, the ratio Selleck AZD3965 of the mRNA expression between AQP4 and H+/K+-ATPase were higher in the H2R knockout mouse regardless of the aging period compared with wild type (Fig. 2c). To summarize these data, the mucosal hyperplasia was induced in the H2R knockout mouse and was aggravated by aging along with the decrease of the mRNA expression of H+/K+-ATPase. The mRNA expression of AQP4 was significantly higher in the H2R knockout mouse but was decreased by aging. The higher ratio of mRNA expression between AQP4 and H+/K+-ATPase was kept

in the H2R knockout mouse, suggesting that the decrease of AQP4 mRNA levels by aging was caused by reduced viability of gastric parietal cells. Subsequently, the influence on H. pylori infection for the gastric mucosal status of SPEM was assessed in wild type or the H2R knockout mice. In the wild type mice, the mRNA expression level of Shh, which is a morphogen for differentiation of gastric mucosal cells, in the stomach was significantly decreased by H. pylori infection (Fig. 3a). PI3K inhibitor In the H2R knockout mouse, the mRNA expression level of Shh

was lower than that of wild type. The mRNA expression learn more level of Shh was the lowest in the H2R knockout mouse with H. pylori infection. The mRNA level of TFF2, which is an indicator of SPEM, was significantly higher in the H2R knockout mouse compared with that of wild type (Fig. 3b). Furthermore, it was increased by H. pylori infection in the wild type and in the H2R knockout mouse. These data suggest that SPEM in the H2R knockout mouse with H. pylori infection would be the most severe among these mice. The fluorescent immunochemistry of AQP4 and H+/K+-ATPase was performed using these mice. In the wild type mice, the infection of H. pylori decreased the expression of AQP4 in the stomach (Fig. 4). Similarly, in the H2R knockout mouse, the infection of H. pylori suppressed the expression of AQP4 as compared with that without the infection of H. pylori, while mucosal hyperplasia with multiple cystic dilatations was observed regardless of the infection of H. pylori. The mRNA expression of AQP4 was significantly decreased by infection of H. pylori in the wild type as well as in the H2R knockout mouse (Fig. 5a). The mRNA expression level of H+/K+-ATPase was also decreased by infection of H.

The construction of mega wind farm projects in the coastal area of this Acalabrutinib mouse region and the increased traffic in their associated ports is of serious concern. In June 2011, the Scientific Committee of the International Whaling Commission strongly

recommended the urgent development of an environmental impact assessment (EIA) for Isla de Chiloé (IWC 2012). Minimum requirements for an effective EIA include the collection, collation, and analysis of appropriate baseline cetacean data, the development of mitigation measures, and the design of a monitoring program aimed to assess impacts against predetermined conservation objectives and to measure the efficacy of any mitigation measures that are implemented. Research should include collection of baseline information on temporal and spatial aspects of cetacean habitat use, population structure, and behavior, and evaluation of all lethal and nonlethal impacts of human activities in an integrated manner, taking into account the cumulative impacts

from all threats and project developments around the area (IWC, in press). Successful mitigation of vessel strikes requires quantitative estimates of strike number, Erlotinib concentration how strike rates change seasonally, where strikes are most likely to occur, and options for minimizing strikes (Vanderlaan et al. 2009). Blue whales (Balaenoptera musculus) should also be included in the EIA because the waters off the northwestern Isla de Chiloé are important feeding habitat for them from late January to early May (Galletti Vernazzani et al. 2012). Our observations highlight the importance of these coastal waters for southern right whales and the need to increase long-term studies, both dedicated and opportunistic, to monitor this critically endangered population. The first interannual resighting of an eastern South Pacific southern right whale and the small number of photo-identified individuals provide additional evidence that this is a small population that deserves its IUCN listing as the “Critically Endangered” Chile-Peru subpopulation (Reilly et al. 2008). The fact that this “subpopulation” is extremely small and several coastal industrial developments may impact it reinforces the

need to implement appropriate management 上海皓元 actions and evaluate their performance as soon as possible. We wish to acknowledge Jaime Conde and Katja Siemund for their valuable contribution with photographs of the recaptured whale; as well as the General Directorate of Maritime Territory and Marine Merchant of the Chilean Navy, Jose Luis Brito from the Natural Science and Archeological Museum of San Antonio and members of the National Marine Mammal Sighting Network for their important collaboration. We would also like to thank Francisco and Miguel Altamirano for their support with the marine survey, Magdalena Altamirano for contributing the videotape showing the reproductive behavior and Roberto Brahm for contributing the video showing the southernmost record of a mother-calf pair.