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Taiwan’s Central Weather Bureau (CWB) has established a new version of tropical cyclone (TC) database to provide users with comprehensive TC data services. As of June 2022, the database includes 1673 TCs originating in the western North Pacific and South China Sea regions since the CWB began TC forecasting operations in 1958. It collects not only the track dataset, satellite imagery, and synoptic weather charts, but also more detailed data and products of TCs that have impacted Taiwan, such as radar reflectivity imagery, high-density surface observations, dropwindsonde data from aircraft observations, and mesoscale analysis maps of rainfall, wind, pressure, and temperature. Such detailed data realistically preserves the TC’s journey across Taiwan and is a feature of the CWB TC database. In addition, the TC database website ( https://rdc28.cwb.gov.tw/TDB/ ) provides tools that allow users to search for TCs of interest based on track, rainfall, and wind. Digital best track data since 1958 is available ( https://rdc28.cwb.gov.tw/TDB/manager/obs_data_download/ ) for users to download and conduct TC research. Also included are technical reports summarizing extensive historical observational research focusing on the mesoscale variations during a TC’s passage over Taiwan. The TC database has been widely used in academic research, disaster prevention, crop revenue insurance, offshore wind power, and other fields. It will continue to develop useful products and integrate more diverse observations to meet the needs of different users.

Taiwan and Philippine (TWPH) (117 - 129°E, 5 - 26°N) is a region with most frequent and intense tropical cyclone (TC) influence in the world. This paper documents the climatology and variability of TWPH TC activity with specific attention to the difference in the TCs formed over the western North Pacific (WNP) and over the South China Sea (SCS). The spatial characteristics of TWPH TCs are analyzed based on the accumulated cyclone kinetic energy (ACE) in four sub-areas where distinctly different TC seasonality and variability is found. Different from over the broad Northwest Pacific Basin (0 - 60°N, 100°E - 180°) where the WNP-born TC frequency dropped sharply in late-1990s and the SCS-born TC frequency slightly increased in mid-1990s, over TWPH three distinct epochs are identified. A weak-variability epoch occurred during 1979 - 1996, a persistent low-ACE epoch during 1997 - 2002, and a more variable epoch during 2003 - 2018. The second epoch is most noteworthy. The unusually weak TC activity during this period in particular over the Philippines was associated with anomalously strong anticyclone over the SCS and the Philippine Sea during the East Asian summer monsoon season. The strong anticyclonic circulation appeared as a descending leg of the enhanced East Asian summer monsoon during summer (July to September). During autumn and early winter (September to December) the Philippine Sea anticyclone was interpreted as the descending Rossby wave response to the suppressed convection over tropical western Pacific. The anomalous anticyclone strengthened the low-level confluent flow and convection over the SCS. The findings are useful to real-time TWPH TC activity monitoring and analysis.

Background Apart from their well-known peripheral cardiovascular effects, emerging evidence indicates that estrogen acts as a modulator in the brain to regulate cardiovascular functions. The underlying mechanisms of estrogen in central cardiovascular regulation, however, are poorly understood. The present study investigated the cardiovascular effects of 17[beta]-estradiol (E2[beta]) in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons are located, and delineated the engagement of nitric oxide (NO) in E2[beta]-induced cardiovascular responses. Methods In male Sprague-Dawley rats maintained under propofol anesthesia, the changes of blood pressure, heart rate and sympathetic vasomotor tone after microinjection bilaterally into the RVLM of a synthetic estrogen, E2[beta] were examined for at least 120 min. The involvement of ER[alpha] and/or ER[beta] subtypes was determined by microinjection of selective ER[alpha] or ER[beta] agonist into bilateral RVLM. Different NO synthase (NOS) inhibitors were used to evaluate the involvement of differential of NOS isoforms in the cardiovascular effects of E2[beta]. Results Bilateral microinjection of E2[beta] (0.5, 1, or 5 pmol) into the RVLM dose-dependently decreased systemic arterial pressure (SAP) and the power density of the vasomotor components of SAP signals, our experimental index for sympathetic neurogenic vasomotor tone. These cardiovascular depressive effects of E2[beta] (1 pmol) were abolished by co-injection of ER antagonist ICI 182780 (0.25 or 0.5 pmol), but not a transcription inhibitor actinomycin D (10 nmol). Like E2[beta], microinjection bilaterally into the RVLM of a selective ER[beta] agonist 2,3-bis(4-hydroxyphenyl) propionitrile (DPN, 1, 2, or 5 pmol) induced significant decreases in these hemodynamic parameters in a dose-dependent manner. In contrast, the selective ER[alpha] agonist 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole (5 pmol) did not influence the same cardiovascular parameters. Co-administration bilaterally into the RVLM of NOS inhibitor N.sup.G.sup.-nitro-L-arginine methyl ester (5 nmol) or selective inducible NOS (iNOS) inhibitor S-methylisothiourea (25 pmol), but not selective neuronal NOS inhibitor 7-nitroindazole (0.5 pmol) or endothelial NOS inhibitor N5-(1-Iminoethyl)-L-ornithine (2.5 pmol), significantly attenuated the cardiovascular depressive effects elicited by DPN (2 pmol). Conclusion Our results indicate that E2[beta] in the RVLM elicited short-term cardiovascular depressive effects via an ER[beta]-dependent nontranscriptional mechanism. These vasodepressor effects of E2[beta] are likely to be mediated by the iNOS-derived NO in the RVLM.

Background Apart from their well-known peripheral cardiovascular effects, emerging evidence indicates that estrogen acts as a modulator in the brain to regulate cardiovascular functions. The underlying mechanisms of estrogen in central cardiovascular regulation, however, are poorly understood. The present study investigated the cardiovascular effects of 17β-estradiol (E2β) in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons are located, and delineated the engagement of nitric oxide (NO) in E2β-induced cardiovascular responses. Methods In male Sprague-Dawley rats maintained under propofol anesthesia, the changes of blood pressure, heart rate and sympathetic vasomotor tone after microinjection bilaterally into the RVLM of a synthetic estrogen, E2β were examined for at least 120 min. The involvement of ERα and/or ERβ subtypes was determined by microinjection of selective ERα or ERβ agonist into bilateral RVLM. Different NO synthase (NOS) inhibitors were used to evaluate the involvement of differential of NOS isoforms in the cardiovascular effects of E2β. Results Bilateral microinjection of E2β (0.5, 1, or 5 pmol) into the RVLM dose-dependently decreased systemic arterial pressure (SAP) and the power density of the vasomotor components of SAP signals, our experimental index for sympathetic neurogenic vasomotor tone. These cardiovascular depressive effects of E2β (1 pmol) were abolished by co-injection of ER antagonist ICI 182780 (0.25 or 0.5 pmol), but not a transcription inhibitor actinomycin D (10 nmol). Like E2β, microinjection bilaterally into the RVLM of a selective ERβ agonist 2,3- bis (4-hydroxyphenyl) propionitrile (DPN, 1, 2, or 5 pmol) induced significant decreases in these hemodynamic parameters in a dose-dependent manner. In contrast, the selective ERα agonist 1,3,5- tris (4-hydroxyphenyl)-4-propyl-1H-pyrazole (5 pmol) did not influence the same cardiovascular parameters. Co-administration bilaterally into the RVLM of NOS inhibitor N G -nitro-L-arginine methyl ester (5 nmol) or selective inducible NOS (iNOS) inhibitor S-methylisothiourea (25 pmol), but not selective neuronal NOS inhibitor 7-nitroindazole (0.5 pmol) or endothelial NOS inhibitor N5-(1-Iminoethyl)-L-ornithine (2.5 pmol), significantly attenuated the cardiovascular depressive effects elicited by DPN (2 pmol). Conclusion Our results indicate that E2β in the RVLM elicited short-term cardiovascular depressive effects via an ERβ-dependent nontranscriptional mechanism. These vasodepressor effects of E2β are likely to be mediated by the iNOS-derived NO in the RVLM.

We present a genome assembly of Caretta caretta (the Loggerhead sea turtle; Chordata, Testudines, Cheloniidae), generated from genomic data from two unrelated females. The genome sequence is 2.13 gigabases in size. The assembly has a busco completion score of 96.1% and N50 of 130.95 Mb. The majority of the assembly is scaffolded into 28 chromosomal representations with a remaining 2% of the assembly being excluded from these.

Estrogen acts on the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons are located, to elicit vasodepressor effects via an estrogen receptor (ER)[beta]-dependent mechanism. We investigated in the present study nontranscriptional mechanism on cardiovascular effects following activation of ER[beta] in the RVLM, and delineated the involvement of phosphatidylinositol 3-kinase (PI3K)/serine/threonine kinase (Akt) signaling pathway in the effects. In male Sprague-Dawley rats maintained under propofol anesthesia, changes in arterial pressure, heart rate and sympathetic neurogenic vasomotor tone were examined after microinjection bilaterally into RVLM of 17[beta]-estradiol (E2[beta]) or a selective ER[alpha] or ER[beta] agonist. Involvement of ER subtypes and PI3K/Akt signaling pathway in the induced cardiovascular effects were studied using pharmacological tools of antagonists or inhibitors, gene manipulation with antisense oligonucleotide (ASON) or adenovirus-mediated gene transfection. Similar to E2[beta] (1 pmol), microinjection of ER[beta] agonist, diarylpropionitrile (DPN, 1, 2 or 5 pmol), into bilateral RVLM evoked dose-dependent hypotension and reduction in sympathetic neurogenic vasomotor tone. These vasodepressive effects of DPN (2 pmol) were inhibited by ER[beta] antagonist, R,R-tetrahydrochrysene (50 pmol), ASON against ER[beta] mRNA (250 pmol), PI3K inhibitor LY294002 (5 pmol), or Akt inhibitor (250 pmol), but not by ER[alpha] inhibitor, methyl-piperidino-pyrazole (1 nmol), or transcription inhibitor, actinomycin D (5 or 10 nmol). Gene transfer by microinjection into bilateral RVLM of adenovirus encoding phosphatase and tensin homologues deleted on chromosome 10 (5 x 10.sup.8 pfu) reversed the vasodepressive effects of DPN. Our results indicate that vasodepressive effects following activation of ER[beta] in RVLM are mediated by nongenomic activation of PI3K/Akt signaling pathway. This study provides new insight in the intracellular signaling cascades involved in central vasodepressive functions of estrogen.

The grizzly bear (Ursus arctos ssp. horribilis) represents the largest population of brown bears in North America. Its genome was sequenced using a microfluidic partitioning library construction technique, and these data were supplemented with sequencing from a nanopore-based long read platform. The final assembly was 2.33 Gb with a scaffold N50 of 36.7 Mb, and the genome is of comparable size to that of its close relative the polar bear (2.30 Gb). An analysis using 4104 highly conserved mammalian genes indicated that 96.1% were found to be complete within the assembly. An automated annotation of the genome identified 19,848 protein coding genes. Our study shows that the combination of the two sequencing modalities that we used is sufficient for the construction of highly contiguous reference quality mammalian genomes. The assembled genome sequence and the supporting raw sequence reads are available from the NCBI (National Center for Biotechnology Information) under the bioproject identifier PRJNA493656, and the assembly described in this paper is version QXTK01000000.

Background Estrogen acts on the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons are located, to elicit vasodepressor effects via an estrogen receptor (ER)β-dependent mechanism. We investigated in the present study nontranscriptional mechanism on cardiovascular effects following activation of ERβ in the RVLM, and delineated the involvement of phosphatidylinositol 3-kinase (PI3K)/serine/threonine kinase (Akt) signaling pathway in the effects. Methods In male Sprague–Dawley rats maintained under propofol anesthesia, changes in arterial pressure, heart rate and sympathetic neurogenic vasomotor tone were examined after microinjection bilaterally into RVLM of 17β-estradiol (E2β) or a selective ERα or ERβ agonist. Involvement of ER subtypes and PI3K/Akt signaling pathway in the induced cardiovascular effects were studied using pharmacological tools of antagonists or inhibitors, gene manipulation with antisense oligonucleotide (ASON) or adenovirus-mediated gene transfection. Results Similar to E2β (1 pmol), microinjection of ERβ agonist, diarylpropionitrile (DPN, 1, 2 or 5 pmol), into bilateral RVLM evoked dose-dependent hypotension and reduction in sympathetic neurogenic vasomotor tone. These vasodepressive effects of DPN (2 pmol) were inhibited by ERβ antagonist, R,R-tetrahydrochrysene (50 pmol), ASON against ERβ mRNA (250 pmol), PI3K inhibitor LY294002 (5 pmol), or Akt inhibitor (250 pmol), but not by ERα inhibitor, methyl-piperidino-pyrazole (1 nmol), or transcription inhibitor, actinomycin D (5 or 10 nmol). Gene transfer by microinjection into bilateral RVLM of adenovirus encoding phosphatase and tensin homologues deleted on chromosome 10 (5 × 10 8 pfu) reversed the vasodepressive effects of DPN. Conclusions Our results indicate that vasodepressive effects following activation of ERβ in RVLM are mediated by nongenomic activation of PI3K/Akt signaling pathway. This study provides new insight in the intracellular signaling cascades involved in central vasodepressive functions of estrogen.

The Steller sea lion is the largest member of the Otariidae family and is found in the coastal waters of the northern Pacific Rim. Here, we present the Steller sea lion genome, determined through DNA sequencing approaches that utilized microfluidic partitioning library construction, as well as nanopore technologies. These methods constructed a highly contiguous assembly with a scaffold N50 length of over 14 megabases, a contig N50 length of over 242 kilobases and a total length of 2.404 gigabases. As a measure of completeness, 95.1% of 4104 highly conserved mammalian genes were found to be complete within the assembly. Further annotation identified 19,668 protein coding genes. The assembled genome sequence and underlying sequence data can be found at the National Center for Biotechnology Information (NCBI) under the BioProject accession number PRJNA475770.