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Notes on two crabs (Crustacea, Brachyura, Dynomenidae and Iphiculidae) collected from red coral beds in northern Taiwan, including a new species of Pariphiculus Alcock, 1896
Peter K. L. Ng‡, M.-S. Jeng§
‡ National University of Singapore, Singapore, Singapore
§ Academia Sinica, Taipei, Taiwan
Corresponding author: Peter K. L. Ng ( peterng@nus.edu.sg )
Academic editor: Sammy De Grave
© 2017 Peter K. L. Ng, M.-S. Jeng.
This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Citation: Ng PKL, Jeng M-S (2017) Notes on two crabs (Crustacea, Brachyura, Dynomenidae and Iphiculidae) collected from red coral beds in northern Taiwan, including a new species of Pariphiculus Alcock, 1896. ZooKeys 694: 135-156. https://doi.org/10.3897/zookeys.694.14871
ZooBank: urn:lsid:zoobank.org:pub:C6FB5FE4-A6F0-47A4-AFBA-3ABC59350D07
Two brachyuran species of the families Dynonemidae and Iphiculidae are reported from red coral beds in northern Taiwan. The dynonemid Acanthodromia margarita (Alcock, 1899) has hitherto been reported from the Andaman Sea, Japan, and Philippines and the species is here recorded for the first time from Taiwan. A new species of iphiculid, Pariphiculus stellatus sp. n., is also described. The new Pariphiculus, which also occurs in the Philippines, is superficially similar to P. agariciferus Ihle, 1918, a species known from Indonesia, Japan, Philippines, South China Sea, Taiwan, and Vanuatu, but can be distinguished by distinct carapace, pleonal and male first gonopod features.
Brachyuran crab, Dromioidea, East China Sea, Leucosioidea, new Pariphiculus species, taxonomy
The small seamount associated with Peng-Chia-Yu Island, a small outcrop 60 km northeast of Keelung in Taiwan, is a special area with controlled commercial fishing for precious red corals (MOJ 2014). One endemic new species, Corallium carusrubrum Tu, Dai & Jeng, 2012 (Anthozoa: Octocorallia: Coralliidae) was recently described from this site.
Recently, two crab species were obtained from the area where the precious red corals are collected. One is the rarely reported dromioid Acanthodromia margarita (Alcock, 1899) (Dynomenidae), hitherto reported from India, Japan, and Philippines. The second is a new species of leucosioid of the genus Pariphiculus Alcock, 1896 (Iphiculidae), which is superficially similar to P. agariciferus Ihle, 1918, from Indonesia, Japan, Philippines, South China Sea, Taiwan, and Vanuatu. The taxonomy of these two species is discussed. The new species of Pariphiculus, here named P. stellatus, is described and compared at length with P. agariciferus. Pariphiculus stellatus sp. n. is also reported from the Philippines.
The measurements provided (in millimetres) are of the maximum carapace width and length (including spines), respectively. The abbreviations G1 and G2 are used for the male first and second gonopods, respectively.
Specimens examined are deposited in the collections of the Institute of Zoology, Biodiversity Research Center, Academia Sinica (ASIZ), Taipei, Taiwan; Muséum national d'Histoire naturelle (MNHN), Paris, France; and the Zoological Reference Collection (ZRC) of the Lee Kong Chian Natural History Museum, National University of Singapore. The terminology used follows that in Tan and Ng (1995) and Davie et al. (2015).
Family Dynomenidae Ortmann, 1892
Genus Acanthodromia A. Milne-Edwards, 1880
Acanthodromia margarita (Alcock, 1899)
Figs 1A–C, 2, 3
Dynomene margarita Alcock, 1899: 19, pl. 2: fig. 3.
Acanthodromia margarita – Alcock 1900: 134; Sakai 1965: 43; Sakai 1976: 31, pl. 7: fig. 2; Nagai 1989: 43; McLay 1999: 539, fig. 31; Marumura and Kosaka 2003: 20; McLay and Ng 2005: 18, fig. 5; Ng et al. 2008: 37.
Material examined
Taiwan: 1 female (17.8 × 18.3 mm) (ASIZ 75484), waters of Zone A (precious coral fishing ground), Peng-Chia-Yu Island, 60 km northeast of Keelung, 25°37.901'N, 122°28.577'E, 175 m, Taiwan, coll. Fishing Vessel "De-Cheng 136", M.-L. Chang, 14 May 2017. Philippines: 1 male (14.7 × 17.7 mm) (ZRC 2001.358), Balicasag Island, 200–300 m, coll. December 2000; 1 male (10.5 × 11.5 mm), 2 females (7.8 × 8.3 mm, 11.2 × 12.2 mm), 2 ovigerous females (14.7 × 16.7 mm, 17.0 × 18.5 mm) (ZRC 2003.668), 1 male (9.9 × 10.6 mm), 1 female (12.3 × 13.4 mm) (MNHN); Balicasag Island, 200 –300 m, 25 –30 Jul 2003; 1 male (14.7 × 15.8 mm) (ZRC 2008.1425), station PN1, Balicasag Island, 200–300 m, coll. November 2003; 1 female (no pereopods left, 11.2 × 12.0 mm) (ZRC 2008.1426), Balicasag Island, 200–300m, coll. November 2003–April 2004; 1 male (15.3 × 16.7 mm) (ZRC 2008.1419), station PN1, Balicasag Island, coll. 29 May 2004; 1 female (17.7 × 19.2 mm) (ZRC 2008.1420), Balicasag Island, coll. 29 March 2004; 5 males (8.8 × 10.6 mm, 11.2 × 12.5 mm, 11.3 × 13.0 mm, 13.5 × 14.2 mm, 14.1 × 16.2 mm), 2 females (15.4 × 17.2 mm, 15.8 × 17.0 mm), 1 female (carapace cracked) (ZRC 2004.596), Balicasag Island, coll. 2 March 2004; 1 male (11.3 × 12.7 mm) (ZRC 2008.1043), Balicasag Island, coll. May 2004 [all above locations at 9.518891°N, 123.680511°E, Panglao, Bohol, Visayas, Philippines; purchased from local shell fishermen, obtained by tangle nets]; 1 male (13.9 × 15.3 mm), 2 females (14.2 × 15.0 mm, 15.7 × 16.1 mm) (ZRC 2013.372), Maribojoc Bay, Panglao, Bohol, Philippines, coll. J. Arbasto, 30 May 2004; 1 female (14.2 × 15.0 mm) (ZRC 2007.207), Maribojoc Bay, Panglao, Bohol, Philippines, coll. J. Arbasto, July-May 2005.
Colour. McLay and Ng (2005: 18) described the fresh colour of Philippine specimens as "light pink spines on carapace and the pereopods with golden yellow dactyli". The present Taiwan specimen is orange-yellow on all its dorsal surfaces, with the spines orange-pink with white tips (Fig. 1A, B). In some Philippine specimens, the carapace can be a more striking pink and the pereopods orange-yellow with the spines pink (Fig. 1C).
Colour in life. A, B Acanthodromia margarita (Alcock, 1899), female (17.8 × 18.3 mm) (ASIZ 75484), Taiwan C Acanthodromia margarita (Alcock, 1899), female (17.7 × 19.2 mm) (ZRC 2008.1420), Philippines D Pariphiculus agariciferus, Ihle, 1918, male (11.9 × 12.1 mm) (ZRC 2009.471), Vanuatu E, F Pariphiculus stellatus sp. n., holotype male (27.7 × 24.5 mm) (ASIZ 75485), Taiwan. A, C, D, E overall dorsal view; B, F ventral view.
The present female specimen from Taiwan is one of the largest on record and agrees well with published descriptions and figures of the species. The frontal margin appears to vary in form due to the relative strength of the frontal spines, particularly the median pseudorostral one. The two large rounded, basally fused tubercles on pleonal somite 4 is distinct in both sexes; with those in some of the smaller specimens appearing almost completely fused, forming one structure (Fig. 3B). The posterior margin of the epistome always has four spines, but the structure of the two median ones varies slightly, from directly pointing downwards (e.g., McLay and Ng 2005: fig. 5B) to curving medially (Fig. 2C).
Acanthodromia margarita (Alcock, 1899), female (17.8 × 18.3 mm) (ASIZ 75484), Taiwan. A overall dorsal view B ventral view of cephalothorax C frontal view of cephalothorax D pleon showing tubercles on somite 4 E outer view of left third maxilliped F outer view of right chela G sublateral view of fingers of right chela.
Acanthodromia margarita (Alcock, 1899). A, B male (11.6 × 12.0 mm) (ZRC 2003.668), Philippines C, male (13.5 × 14.2 mm) (ZRC 2004.596), Philippines. A overall dorsal view B, C pleon showing tubercles on somite 4.
Distribution and depth
Acanthodromia margarita was described from the Andaman Sea in the eastern Indian Ocean, and has been also reported from Japan, Philippines, and now Taiwan. The Indian Ocean specimen was from relatively shallow water (135 m), but the series from the Philippines was from 120–300 m depth. The present Taiwan specimen was collected from a depth of 175 m.
Pariphiculus agariciferus Ihle, 1918, overall dorsal view. A holotype male (9.0 × 9.3 mm), after Ihle (1918: fig. 230) B young male (10.2 × 9.6 mm) (ZRC 2009.470), Vanuatu C male (11.9 × 12.1 mm) (ZRC 2009.471), Vanuatu D female (22.1 × 21.3 mm) (ZRC 2009.288), Philippines E male (15.5 × 14.4 mm) (ZRC 2012.484), Philippines F female (19.0 × 19.0 mm) (ZRC 2017.186), Philippines.
Pariphiculus agariciferus Ihle, 1918. A, B female (19.8 × 18.9 mm) (ZRC 2017.181), Philippines C male (15.5 × 14.4 mm) (ZRC 2012.484), Philippines D young male (10.2 × 9.6 mm) (ZRC 2009.470), Vanuatu E male (11.9 × 12.1 mm) (ZRC 2009.471), Vanuatu F male (15.8 × 15.0 mm) (ZRC 2017.187), Philippines G, I female (22.1 × 21.3 mm) (ZRC 2009.288), Philippines H female (19.0 × 19.0 mm) (ZRC 2017.186), Philippines. A, B outer view of right third maxilliped C–E male thoracic sternum and pleon E female thoracic sternum and pleon G, H female thoracic sternum and pleon E female thoracic sternum and pleon I right fourth ambulatory leg.
Pariphiculus agariciferus Ihle, 1918. A male (11.9 × 12.1 mm) (ZRC 2009.471), Vanuatu B male (15.8 × 15.0 mm) (ZRC 2017.187), Philippines C, J male (15.5 × 14.4 mm) (ZRC 2012.484), Philippines D male (12.8 × 13.7 mm) (ZRC 2017.186), Philippines E, G female (19.0 × 19.0 mm) (ZRC 2017.186), Philippines F, H female (22.1 × 21.3 mm) (ZRC 2009.288), Philippines I male (11.9 × 12.1 mm) (ZRC 2009.471), Vanuatu. A–F intestinal region and posterior margin of carapace G, H outer view of left chela I, J outer view of right chela.
Family IPHICULIDAE Alcock, 1896
Pariphiculus Alcock, 1896
Pariphiculus stellatus sp. n.
http://zoobank.org/7EC3869E-1F27-4C50-8EE3-DCEB4817630C
Figs 7, 8, 9, 10, 11B, D, F, 12B, D, F, 13E–H
Pariphiculus sp. – Ikeda 1998: 84, pl. 2.
Pariphiculus agariciferus – Galil and Ng 2007: 87 (part) (not Pariphiculus agariciferus Ihle, 1918).
Holotype: male (27.7 × 24.5 mm) (ASIZ 75485), waters of Zone A (precious coral fishing ground), Peng-Chia-Yu Islands, 60 km northeast of Keelung city, 25°37.765'N, 122°28.623'E, 170 m, Taiwan, coll. Fishing Vessel "De-Cheng 136", M.-L. Chang, 7 May 2017. Philippines: Non-types: 1 female (31.1 × 26.2 mm) (ZRC 2017.188), Balicasag Island, coll. J. Arbasto, July 2004–May 2005; 1 male (24.3 × 21.6 mm), 1 female (35.1 × 29.6 mm) (ZRC 2007.590), Balicasag Island, coll. 2 March 2004; 1 male (15.4 × 13.8 mm) (ZRC 2017.184), station PN1, Balicasag Island, coll. November 2003; 1 female (32.3 × 27.6 mm) (ZRC 2017.185), Balicasag Island, Panglao, Philippines, 80–140 m, in tangle nets, coll. March 2004 [all above locations at 9.518891°N, 123.680511°E, Panglao, Bohol, Visayas, Philippines; purchased from local shell fishermen, obtained by tangle nets].
Comparative material of Pariphiculus agariciferus Ihle, 1918
Taiwan: 1 male (12.9 × 12.3 mm) (ASIZ 75113), 22°14.74'N, 118°43.69'E 141 m, southern Taiwan, coll. M.-L. Chang, 14 May 2011. Philippines: 1 male (16.6 × 16.2 mm) (ZRC 2015.436), Balicasag Island, coll. J. Arbasto, July 2004–May 2005; 2 females (19.5 × 18.9 mm, 19.8 × 18.9 mm) (ZRC 2017.181), Balicasag Island, coll. J. Arbasto, 2006; 1 female (19.3 × 17.6 mm), 1 broken female (ZRC 2001.559), Balicasag Island, 50–500 m, coll. 28 November 2001; 1 male (14.4 × 13.3 mm), 1 female (21.0 × 19.1 mm) (ZRC 2009.297), Balicasag Island, coll. June 2002; 2 males (13.4 × 13.3 mm, 15.8 × 15.8 mm), 1 female (19.5 × 18.4 mm) (ZRC 2007.588a), station PN1, Balicasag Island, coll. November 2003; 1 male (13.9 × 13.3 mm) (ZRC 2009.1164), Balicasag Island, coll. December 2003; 1 female (16.6 × 18.6 mm) (ZRC 2017.180), station P2, Balicasag Island, 2004; 1 male (14.0 × 13.5 mm) (ZRC 2015.437), Balicasag Island, coll. 2 March 2004; 1 male (15.8 × 15.0 mm) (ZRC 2017.187), Balicasag Island, Panglao, Philippines, 80–140 m, in tangle nets, coll. March 2004; 1 male (15.5 × 14.4 mm) (ZRC 2012.484), Balicasag Island, coll. May 2004; 1 female (22.0 × 21.6 mm) (ZRC 2017.183), station P1, Balicasag Island, coll. 6 July 2004; 1 young female (15.0 × 14.7 mm) (ZRC 2017.182), station P4, Balicasag Island, coll. 2 July 2004; 2 females (18.4 × 18.0 mm, 22.1 × 21.3 mm) (ZRC 2009.288), Balicasag Island, coll. J. Arbasto, July 2004–May 2005; 1 male (12.8 × 13.7 mm), 1 female (19.0 × 19.0 mm) (ZRC 2017.186), Balicasag Island, Panglao, Philippines, 80–140 m, in tangle nets, coll. J. Arbasto, 2004–2005; 1 male (15.4 × 16.0 mm) (ZRC 2009.185), Balicasag Island, 120–160 m, coll. J. Arbasto, January–December 2007 [all above locations at 9.518891°N, 123.680511°E, Panglao, Bohol, Visayas, Philippines; purchased from local shell fishermen, obtained by tangle nets]; 1 male (17.2 × 16.9 mm), 2 females (16.1 × 15.4 mm, 18.5 × 18.7 mm) (ZRC 2013.104), Maribojoc Bay, Panglao, Bohol, Philippines, coll. J. Arbasto, November 2003–April 2004. Vanuatu: 1 male (10.2 × 9.6 mm), 1 female (13.0 × 13.5 mm) (ZRC 2009.470), station AT13, south of Aésé Island, Palikulu Bay, 15°27.8S 167°15.7E, 146–153 m, Santo, coll. N.O."Alis", SANTO Expedition, 19 September 2006; 1 male (11.9 × 12.1 mm) (ZRC 2009.471), station AT61, south of Urélapa Island, West Malo Island, 15°39'S 167°01'E, 266–281 m, Santo, coll. N.O."Alis", SANTO Expedition, 4 October 2006; 2 juvenile females (10.3 × 9.4 mm, 13.4 × 13.6 mm), 1 carapace only (17.9 × 17.4 mm) (ZRC 2009.472), station AT63, south of Urélapa Island, West Malo Island, 15°40'S 167°01'E, 290–334 m, Santo, coll. N.O."Alis", SANTO Expedition, 4 October 2006; 1 male (11.9 × 11.8 mm) (ZRC 2009.473), station AT64, south of Urélapa Island, West Malo Island, 15°40'S 167°02'E, 249–252 m, Santo, coll. N.O."Alis", SANTO Expedition, 19 September 2006.
Carapace 1.12–1.19 times broader than long; with relatively low mushroom-shaped tubercles on carapace, chelipeds and ambulatory legs with margins of tops distinctly asteriform (Figs 7, 8A, G, 9A, B, 11D, F, 12B); gastric and branchial regions inflated (Figs 8A, G, 11D, F); in lateral view, surface behind postfrontal region gently concave, forming shallow depression (Fig. 11F); suborbital tubercle relatively low, not protruding (Figs 8A, G, 9C, 11D); palms of chelae relatively long, slender, with fingers long, gently curved (Figs 9E–H, 12F); dorsal margin of dactylus and ventral margin of pollex of chela lined with low granules, never serrated (Figs 9E–H, 12F); tubercles and granules on surface of male and female pleons relatively large, tend to be fused, forming semi-eroded structures (Figs 8D, E, 9D, 12D); male telson proportionately shorter (Figs 8D, E, 12D); G1 relatively long, slender (Fig. 13E).
Pariphiculus stellatus sp. n. A, C–E holotype male (27.7 × 24.5 mm) (ASIZ 75485), Taiwan B female (32.3 × 27.6 mm) (ZRC 2017.185), Philippines F male (24.3 × 21.6 mm) (ZRC 2007.590), Philippines G female (35.1 × 29.6 mm) (ZRC 2007.590), Philippines. A, B, F, G overall dorsal view C–E dorsal view of carapace photographed from slightly different angles.
Pariphiculus stellatus sp. n. A–F holotype male (27.7 × 24.5 mm) (ASIZ 75485), Taiwan G, H male (24.3 × 21.6 mm) (ZRC 2007.590), Philippines. A, G frontal view of cephalothorax showing orbit, antennae, antennules and buccal cavity B, C outer view of left third maxilliped D, H male thoracic sternum and pleon E male pleon F left third ambulatory leg.
Description of male
Carapace 1.12–1.19 times broader than long, regions not well-defined; dorsal surface with numerous low mushroom-shaped tubercles and granules, edges of raised tubercle with short slender spinules, asteriform from dorsal view, with scattered short setae between them; postfrontal region raised, prominent; surface behind postfrontal region with shallow depression; gastric regions convex, separated from swollen branchial regions by shallow, partially granulated groove; branchial regions with numerous large and small tubercles, separated from intestinal and cardiac regions by relatively broad granulated groove; cardiac and intestinal regions barely distinguishable, intestinal region with 2 prominent large tubercles, one dorsal in position, another directed obliquely posteriorly; hepatic region gently concave, with distinct low lateral tubercle, surface granulated; pterygostomial and suborbital regions with numerous mushroom-shaped, asteriform tubercles; branchiostegite region with numerous low, rounded tubercles (Figs 7, 8A, G, 9A–C, 11B, D–F, 12B). posterolateral border adjacent to cardiac region prominently protruded to form large tooth. Front slightly produced, not protruding beyond anterior edge of buccal cavity and closed third maxillipeds, gently upturned, weakly bilobed (distinct in frontal view) (Figs 7, 8A, G, 11B, D, 12B). Antero- and posterolateral margins not cristate, not clearly demarcated, with structures gradually merging medially on carapace; subdorsal margins lined with numerous large mushroom-shaped tubercles with asteriform tops, with interspersed smaller granules of similar form; posterior carapace margin with 3 broad, stout tubercles, each covered with smaller granules, median one smallest (Figs 7, 9A, B, 11B, 12B).
Pariphiculus stellatus sp. n. A, C, E holotype male (27.7 × 24.5 mm) (ASIZ 75485), Taiwan B female (32.3 × 27.6 mm) (ZRC 2017.185), Philippines F male (24.3 × 21.6 mm) (ZRC 2007.590), Philippines D, G, H female (35.1 × 29.6 mm) (ZRC 2007.590), Philippines. A, B intestinal region and posterior margin of carapace C antennae, antennules and orbit D female thoracic sternum and pleon E, F, H outer view of left chela G outer view of right chela. Abbreviation: stu = suborbital tubercle.
Pariphiculus stellatus sp. n. A holotype male (27.7 × 24.5 mm) (ASIZ 75485), Taiwan B female (31.1 × 26.2 mm) (ZRC 2017.188), Philippines. A male sternopleonal cavity showing right G1 and pleonal locking tubercle on sternite 5 B female sternopleonal cavity showing vulvae on sternite 6.
Basal article of antenna subquadrate, surface gently convex, fused with epistome; short flagellum lodged in orbital hiatus (Fig. 9C). Basal segment of antennule occupies entire fossa when closed, with folded articles hidden behind basal article; margins of fossae almost smooth (Figs 8A, G, 9C). Orbit rounded; eyes small with short ocular peduncle, mobile; suborbital tubercle relatively low, not prominent, asteriform (Figs 8A, G, 9C, 11D).
Third maxillipeds relatively short; outer surfaces of merus, ischium, basis and exopod densely covered with mushroom-shaped tubercles and granules, many with asteriform tops; merus triangular with broadly pointed apex, inner edge straight, outer edge gently convex, with large, low rounded tubercle on proximal margin; ischium ca. 2 times longer than merus along inner margin, with prominent submedian ridge of tubercles; palp (carpus, propodus and dactylus, short, completely hidden behind ischium when folded; exopod relatively broad, reaching beyond distal margin of ischium, tip rounded, without flagellum (Figs 8B, C, G 11D).
Chelipeds slender, elongate, subequal; surfaces with numerous large, round or low mushroom-shaped tubercles, some with asteriform tops (Figs 7A, F, G, 9E–H, 11B, 12F). Merus cylindrical in cross-section; carpus small, subtriangular (Figs 7A, F, G, 9E–H, 11B). Chela with proximal half relatively stouter, gradually tapering to more slender distal part, margins granulated but not serrated; fingers elongate, just longer than palm, surface with very small granules, gently curved, distal two-thirds more darkly pigmented, rest of structure white in preservative; cutting edges of both fingers with long and short sharp vertical spines (Figs 9E–H, 12F).
Ambulatory legs relatively short, first leg longest; surfaces of merus, carpus and propodus covered with small rounded or mushroom-shaped tubercles, some with asteriform tops (Figs 7A, F, G, 8F, 11B); dactylus styliform, almost straight, surfaces smooth, margins lined with setae (Fig. 8F).
Thoracic sternum relatively narrow transversely; surfaces of sternites 1–4 covered with round or low mushroom-shaped tubercles, some with asteriform tops, some coalescing to form ridges and clusters; surfaces of sternites 5–8 with more individual tubercles and granules; sternites 1 and 2 separated by low ridge, longitudinally very narrow, lateral surfaces of sternite 2 with thick row of coalesced tubercles; separated from coalesced row of tubercles on sternite 3 by deep groove; tubercles on sternite 3 separated from cluster of coalesced tubercles on sternite 4 by deep groove; sternites otherwise not clearly demarcated; small part of sternite 8 just visible when pleon closed; sternopleonal cavity narrow, deep, nearly reaching buccal cavity at level of sternite 2 (Figs 8D, H, 12D); all sutures from sternites 3–8 medially interrupted; peg-like tubercle of pleonal locking mechanism relatively large, semicircular, directed anteriorly (Fig. 10A); penis short, tubular with dilated tip, arising from condyle of coxa of fourth ambulatory leg (Fig. 10A).
Comparisons between similar sized Pariphiculus agariciferus Ihle, 1918, and P. stellatus sp. n. A, C, E P. agariciferus, male (15.8 × 15.8 mm) (ZRC 2007.588), Philippines B, D, F P. stellatus, male (15.4 × 13.8 mm) (ZRC 2017.184), Philippines [left frontal margin damaged]. A, B overall dorsal view C, D frontal view of cephalothorax showing orbit, antennae, antennules and buccal cavity E, F right lateral view of cephalothorax. Abbreviation: stu = suborbital tubercle.
Comparisons between similar sized Pariphiculus agariciferus Ihle, 1918, and P. stellatus sp. n. A, C, E P. agariciferus, male (15.8 × 15.8 mm) (ZRC 2007.588), Philippines B, D, F P. stellatus, male (15.4 × 13.8 mm) (ZRC 2017.184), Philippines [telson missing, approximate shape and proportions as indicated by space on sternopleonal cavity]. A, B intestinal region and posterior margin of carapace C, D male thoracic sternum and pleon (somite 6 damaged and telson missing in D) E, F outer view of right chela.
Pleon triangular, covered with large rounded tubercles, many coalescing to form semi-eroded structure on somites 1–6; surface of telson with scattered small, narrow mushroom-shaped; somites 1, 2 free; somites 3–5 functionally fused although somites can still be approximately distinguished; somites 2–6 trapezoidal; somite 6 free, broadly subrectangular with lateral margin convex; telson triangular, elongate; surface of somite 3 with subrectangular cluster of fused granules; surface of somite 2 with 3 uneven clusters of fused granules (Figs 8D, E, H, 12D).
G1 ca. 2 times length of G2, relatively slender, slightly sinuous basally, becoming almost straight distally; margins lined with dense soft long setae; tip sharp (Fig. 13E–G). G2 with with elongate subpetaloid terminal process which is slightly shorter than basal segment (Fig. 13H).
Females and variations
Female specimens are similar to males in almost all non-sexual aspects. The female pleon is of the typical iphiculid condition, with all the somites and telson freely articulating, none swollen or forming a dome-like structure covering the egg mass (Fig. 9D). The vulva is relatively small and simple with around opening, covered by an operculum, and directed obliquely posteriorly (Fig. 10B). Small specimens have proportionately shorter meri of the chelipeds although in all other aspects, the structures are similar (Figs 7B, F, 11B).
The fresh holotype of P. stellatus was a dull orange throughout, with some of the large posterior tubercles white; the distal two-thirds of fingers bright orange and basal third cream (Fig. 1E). The ventral surfaces are generally dirty white to light brown (Fig. 1F). A relatively larger fresh specimen of P. agariciferus (18. 1 mm carapace width) was figured by Galil and Ng (2007: fig. 3B) and its colour was similar to that of P. stellatus, being orange throughout. A smaller male specimen from Taiwan (12.9 × 12.3 mm, ASIZ 75113), however, had most of the carapace and chelipeds white and pale orange (Shih et al. in press). A similar sized male from Vanuatu (11.9 × 12.1 mm, ZRC 2009.471) had a similar colour pattern as the Taiwan specimen except that the colour is more intense (Fig. 1D)
The species is named after the prominent asteriform or "star-like" mushroom-shaped tubercles and granules on the carapace and chelipeds.
The large specimen from Taiwan is interesting as it is almost identical with a large female specimen measuring 36.2 × 30.3 mm figured by Ikeda (1998: 84) from Sagami Bay which he identified as "Pariphiculus sp.". Ng (1999: 718), in his review of the book, noted that this was almost certainly a new species although he incorrectly suggested it may be a species of Parilia Wood-Mason in Wood-Mason & Alcock, 1891, instead. Examination of the present Taiwanese specimen suggests it is close to Pariphiculus agariciferus Ihle, 1918, a species known from Indonesia, Japan, Philippines, Taiwan, South China Sea and Vanuatu (Ihle 1918: 250; Balss 1922: 131; Yokoya 1933: 129; Sakai 1937: 131; Sakai 1965: 43; Serène and Vadon 1981:124; Sakai 1976: 104; Chen 1989: 231; Tan 1996: 1023; Komatsu et al. 2005: 106; Galil and Ng 2007: 87; Galil and Ng 2010: 143; Ng et al. 2008: 37; Shih et al. in press). The size of the Taiwanese (and Ikeda's Japanese) specimen, however, is much larger (almost twice) that what is known for P. agariciferus which averages 15–20 mm in carapace width. The Taiwanese specimen differs from typical P. agariciferus in a number of carapace, cheliped, male pleonal and G1 characters that suggests that it is a different taxon, but its large size makes comparisons difficult.
Fortunately, there is a good series of specimens of what had been identified as "P. agariciferus" from Philippines and Vanuatu by Galil and Ng (2007, 2010), as well as additional material in the ZRC not reported by them. While the majority of the specimens are P. agariciferus s. str., there are several specimens mixed among this material (cf. Galil and Ng 2007) that are clearly conspecific with the Taiwan specimen. This includes a small male specimen of the new species which allows for size-equivalent comparisons between the two taxa to be made. We can now be confident that the present Taiwanese male, Ikeda's (1998) specimen, and some of the Philippine material represent a new species, here named Pariphiculus stellatus sp. n.
Pariphiculus agariciferus Ihle, 1918, is a smaller species, with all specimens less than 22 mm in carapace length. The holotype male from seas around Timor and Rotti islands in Indonesia measured 9.0 × 9.3 mm (not measured to tip of spines). The carapace of the holotype male has all the lateral spines relatively slender and long, all of which are covered with additional spinules and tubercles; with the tubercles and granules on the carapace and chelipeds mushroom-shaped (Fig. 4A). A slightly larger male from Vanuatu has a very similar in carapace morphology (Fig. 4B). These characters are almost certainly juvenile features; the small Vanuatu specimen is still subadult, with the gonopods poorly chitinised; and the holotype male is probably a young individual as well. In the larger male specimens from the Philippines, Taiwan and Vanuatu, the lateral spines (including those on the posterior carapace margin) are relatively shorter and stouter (Figs 4C–F, 6A–F). The ambulatory meri and dactyli of the smallest specimens are also proportionately more slender and elongate (Fig. 4A, B). As specimens get larger (regardless of sex), the carapace becomes proportionately wider and rounder, and the spines shorter and blunter (Fig. 4C–F). The ambulatory meri and dactyli of these larger specimens are also relatively stouter and shorter (Fig. 4C–F). As the specimens increase in size, the tops of the mushroom-shaped tubercles on the carapace and chelae also become more mushroom-shaped, with the margins more gently serrated and distinctly asteriform (Figs 4C–F, 6A–F).
Pariphiculus stellatus sp. n. can be distinguished from P. agariciferus in having the gastric and branchial regions of the carapace proportionately less inflated (Figs 8A, G, 11D, F) (vs. prominently inflated in frontal view in P. agariciferus; cf. Fig. 11C, E); the tubercles on the carapace, chelipeds and third maxillipeds are prominently mushroom-shaped but relatively lower, with the tops of the large tubercles distinctly asteriform (Figs 8A–C, G, 9A, B, 11D, F, 12B) (vs. tubercles on the carapace are relatively higher and mushroom-shaped, with the margins of the tops of the tubercles uneven but not distinctly asteriform in P. agariciferus; cf. Figs 5A, B, 6A–F, 11C, E, 12A); in lateral view, the surface behind the postfrontal region is gently concave, forming a shallow depression (Fig. 11F) (vs. area behind postfrontal region deeply concave, with a marked depression between frontal and gastric regions in P. agariciferus; cf. Fig. 11E); the suborbital tubercle is relatively low, not protruding and not conspicuous (Figs 8A, G, 9C, 11D) (vs. suborbital tubercle is large and prominently protrudes anteriorly in P. agariciferus; cf. Fig. 11C); the palms of the chelae are relatively long, slender with the fingers gently curved (Figs 9E–H, 12F) (vs. palms relatively short, swollen with the fingers distinctly curved in P. agariciferus; cf. Figs 6G–J, 12C); the dorsal margin of the dactylus and ventral margin of the pollex of the chela is lined with low granules, never serrated (Figs 9E–H, 12F) (vs. non-cutting margins of dactylus and pollex with prominent sharp and/or mushroom-shaped granules, appears serrated in P. agariciferus; cf. Figs 6G–J, 12C); the tubercles and granules on the surface of the male and female pleons are larger, tend to be fused, forming semi-eroded structures (Figs 8D, E, H, 9D, 12D) (vs. tubercles and granules tend to be smaller, discrete and packed in P. agariciferus; cf. Figs 5C–H, 12C); the male telson is proportionately shorter, even in small specimens (Figs 8D, E, H, 12D) (vs. male telson more elongate in P. agariciferus; cf. Figs 5C–F, 12C); and the G1 is relatively longer and more slender (Fig. 13E) (vs. G1 proportionately stouter and shorter in P. agariciferus; cf. Fig. 13A). It is important to note also that the single male specimen of P. stellatus sp. n. (Figs 11B–F, 12B–F) similar in size to adult P. agariciferus (Figs 11A, C, E, 12A, C, E) is still subadult, with the G1 soft and not well developed.
All the specimens of P. stellatus sp. n. have been collected by tangle nets in Taiwan and the Philippines. This is also true for all the P. agariciferus collected from the Philippines, with only a few specimens obtained by trawls (e.g. those in Vanuatu and Taiwan). The material from the Philippines was collected from deeper waters along steep cliffs, areas which can neither be sampled by divers, trawls or dredges (Ng et al. 2009). These heretofore rare species almost certainly prefer such inaccessible habitats and are thus rarely collected by dredges and trawls (see Mendoza et al. 2010).
Gonopods. A–D Pariphiculus agariciferus Ihle, 1918, male (15.8 × 15.0 mm) (ZRC), Philippines E–H P. stellatus sp. n., holotype male (27.7 × 24.5 mm) (ASIZ 75485), Taiwan. A–C, E–G left G1 D, H left G2. Scale bars A, E, D, H 1.0 mm; B, C, F, G 0.5 mm.
Ikeda's (1998) Japanese specimen was collected from 180–200 m of water off Nagai in Sagami Bay. The holotype male from Taiwan was obtained from a depth of 170 m, with the series from the Philippines collected from 80–140 m.
This study was partially sponsored by the Fisheries Agency, Council of Agriculture, Executive Yuan, R.O.C. (106AS-10.2.1-FA-F1). We are grateful to Bella Galil, Hironori Komatsu, and Sammy De Grave for their many constructive comments. Thanks are also due to Cheng Anyi (ASIZ) for her help with the manuscript.
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text:
Hereditary Factor I Deficiency
Hypofibrinogenemia
Congenital fibrinogen deficiency (CFD) is a rare, hereditary bleeding disorder. CFD may correspond to a quantitative deficiency of fibrinogen, which is referred to as afibrinogenemia or hypofibrinogenemia, or the production of dysfunctional fibrinogen, warranting the diagnosis of dysfibrinogenemia. Patients suffering from afibrinogenemia, hypofibrinogenemia, or certain types of dysfibrinogenemia present a hemorrhagic diathesis. On the other hand, dysfibrinogenemia may also be associated with thrombophilia.
In 85% of all cases, congenital afibrinogenemia manifests in umbilical cord bleeding. Otherwise, the child's propensity to bleed is observed in the neonatal period. While mucosal hemorrhages resulting in epistaxis or bleeding gums are frequently reported, blood loss from the gastrointestinal tract or urogenital system is rare [1]. Muscle hematomas and hemarthrosis are regularly observed [2] [3], but subcutaneous bleedings and bruises, which are clinical hallmarks of other types of hemophilia, are less common in CFD and affect <50% of all patients [4]. Although unusual, patients with afibrinogenemia are permanently at risk of life-threatening hemorrhages of the central nervous system [2]. Females in fertile age may suffer from menorrhagia or menometrorrhagia, and they may have major difficulties to carry to term. Abortion within the first trimester of pregnancy is commonly described, regardless of the genotype of the unborn child [1] [2].
In general, the severity of CFD depends on the concentration of functional fibrinogen, so that afibrinogenemia is associated with more severe bleeding events than hypofibrinogenemia [2]. Indeed, patients with hypofibrinogenemia tend to remain asymptomatic until trauma occurs [1] [2]. Nevertheless, the presentation of quantitative CFD may vary, even among those individuals with the same genotype. Hypofibrinogenemia may interfere with fertility, prevent women from carrying to term, and has even been related to liver disease [4].
The clinical presentation of dysfibrinogenemia is heterogeneous and ranges from moderate or mild hemophilia to asymptomatic to a tendency to thrombosis [5]. With regard to the latter, deep vein thrombosis, thrombophlebitis, and pulmonary embolism are most frequently reported [2]. Paradoxically, both arterial and venous thrombotic complications have also occasionally been described in patients with afibrinogenemia [6] [7] [8].
Easy Bruising
Afibrinogenemia Common Symptoms nosebleeds (epistaxis) easy bruising heavy or prolonged menstrual bleeding (menorrhagia) muscle bleeds bleeding into joints (hemarthrosis) bleeding from the umbilical cord stump after birth bleeding in the mouth, particularly [wfh.org]
bruising, mucosal bleeding, GI / GU bleeding, hemarthrosis, intracranial hemorrhage, recurrent fetal loss, menorrhagia, menometrorrhagia, placental abruption or postpartum hemorrhage; rarely patients can have hemopericardium, hemoperitoneum or spontaneous [pathologyoutlines.com]
Aside from the fact that women have similar symptoms to men with bleeding disorders (recurrent nosebleeds, easy bruising, bleeding from the digestive or urinary tract and excessive bleeding from the mouth or gums), they can also experience added obstetric [rarediseases.info.nih.gov]
[…] avoided Additional and Relevant Useful Information for Congenital Afibrinogenemia: A fibrinogen blood test is performed if there are symptoms suggestive of a coagulation disorder - either bleeding (from body sites, or from bleeding spots on skin, or easy [dovemed.com]
Hematologic disease Brite Human diseases [BR: br08402 ] Cardiovascular diseases Hematologic diseases H00222 Afibrinogenemia Human diseases in ICD-11 classification [BR: br08403 ] 03 Diseases of the blood or blood-forming organs Coagulation defects, purpura [genome.jp]
Patients with Acute Thrombolytic Therapy Unusual Sites of Arterial Occlusion Pathogenesis and Treatment of BiomaterialAssociated Overview of Complex Thrombohemorrhagic Disorders Consumptive Thrombohemorrhagic Disorders The Thrombotic Thrombocytopenic Purpura [books.google.ro]
Current treatment procedures Infantile hemangiomas are the most common benign tumors Thrombotic microangiopathies – hemolytic-uremic syndromes and thrombotic thrombocytopenic purpura Thrombotic microangiopathies are a heterogeneous group of disease Nonhealing [prolekare.cz]
The patient's propensity to bleed, which is reflected in anamnestic data and clinical observations, warrants the diagnosis of hemophilia. Occurrence at birth or very early in life raises suspicion as to a hereditary disorder, but neither allows for a reliable diagnosis nor for the differentiation of bleeding disorders. Coagulation studies generally serve as the first step towards a clarification of that issue. In this context, platelet count, fibrinogen levels, activated partial thromboplastin time (APTT), prothrombin time (PT), and thrombin time (TT) should be assessed. In case of quantitative CFD, these studies reveal reduced concentrations of fibrinogen and the prolongation of all bleeding times, which rely on the formation of fibrin as their endpoint [2]. Antigen levels may be within reference ranges in patients with dysfibrinogenemia, but bleeding times are also prolonged. Functional assays have to be carried out to demonstrate a qualitative deficiency of fibrinogen, and they should yield a low activity-to-antigen ratio [5].
Despite demographic data indicating a hereditary disease, mixing studies should be carried out to rule out the presence of an inhibitor. In case of CDF, mixing of the patient's plasma with normal plasma will correct abnormal bleeding times. Finally, the diagnosis of CFD may be confirmed by the identification of the underlying mutation. Molecular genetic studies are highly recommended to associate dysfibrinogenemia with a particular phenotype [5].
Fibrinogen Decreased
As fibrinogen decreases under threatened premature labor or inflammation, it is necessary to maintain the fibrinogen level higher than 100 mg/dL during pregnancy [2, 3]. [hindawi.com]
Jugular Venous Pressure
Absent A-Waves
Normal Von Willebrand disease[10] Bernard–Soulier syndrome[9] Normal Normal Normal Decreased or absent Glanzmann's thrombasthenia[9] Afibrinogenemia Decreased Decreased Decreased Normal or decreased Storage pool deficiency[10] Absent second wave Partial [en.wikipedia.org]
Among the causes of spontaneous intrahepatic bleeding, the most common are hepatocellular carcinoma and hepatic adenoma. The diagnosis of hepatocellular carcinoma has been discarded on CT images. [journals.lww.com]
On-demand treatment is indicated in most cases of CFD. However, patients suffering from severe hemophilia and those who experienced life-threatening hemorrhages may benefit from regular administrations of fibrinogen. Weekly or biweekly applications are generally recommended to this end and aim at fibrinogen levels of 0.5-1.0 g/l. In any case, the advantages of prophylactic applications of fibrinogen should be carefully weighed against the threat of thrombosis and thromboembolism [3]. This applies to surgical patients receiving fibrinogen replacement therapy until complete healing and women requiring prolonged treatment during pregnancy. In pregnant women, target plasma levels of fibrinogen are as described above, but higher concentrations should be aimed for during delivery. Ideally, plasma levels are raised to 1.5 g/l then [1] [2] [4].
Symptomatic therapy typically consists in the administration of fibrinogen concentrates, cryoprecipitates, or fresh frozen plasma [1]. It may be complemented by the application of antifibrinolytics or, for local hemostasis, fibrin glue. Estrogen-progestogen preparations are helpful to reduce menstrual blood loss in women suffering from menorrhagia [2] [3].
Thrombotic episodes often require the concurrent use of fibrinogen and anticoagulants like low-molecular-weight heparin, regardless of the underlying type of CFD [2]. No recommendations have been published regarding possible prophylaxis of thrombosis and thromboembolism in patients with prothrombotic dysfibrinogenemia [5].
Umbilical cord bleeding due to afibrinogenemia may be lethal, and significant morbidity and mortality are associated with the thrombotic complications of afibrinogenemia and dysfibrinogenemia [4]. With regards to quantitative CFD and dysfibrinogenemia with a hemorrhagic diathesis, relative protection from major bleeding events is to be expected if plasma fibrinogen concentrations are raised >0.7 g/l, and the risk of life-threatening hemorrhages reduces to negligible values if plasma levels of >1.0 g/l are achieved [2]. Data regarding the long-term outcome of prothrombotic dysfibrinogenemia are not available [5].
Fibrinogen circulates as a heterohexamer consisting of each two Aα chains, Bβ chains, and γ chains. They are encoded by genes FGA, FGB, and FGG, which are all located on the long arm of chromosome 4. Pathogenic mutations resulting in CFD have been described in all three genes and amount to a total of about 200 molecular defects [4] [5]. Afibrinogenemia and hypofibrinogenemia are generally related to null mutations, while missense mutations account for the majority of cases of dysfibrinogenemia [4]. While afibrinogenemia and hypofibrinogenemia are assumed to be inherited in an autosomal recessive manner, most variants of dysfibrinogenemia follow an autosomal dominant mode of inheritance [5].
Doubts remain with regard to the presence of modifier genes that may explain phenotypic differences between individuals with the same genotype. Although no such modifiers could be identified to date, research interests in the molecular background of afibrinogenemia and dysfibrinogenemia haven't declined: Knowledge regarding genotype-phenotype correlations for these conditions may allow for the prediction of bleeding and thrombosis risks, it is hoped. For some types of fibrinogen, such correlations could be recognized: Fibrinogens Caracas V (FGA, c.1595C>G), Chapel Hill III/Dusart/Paris V (FGA, c.1717C>G), Christchurch II/Ijmuiden/London VIII/St-Germain III/Vicenza III (FGB, c.130C>T), New York I (FGB, deletion of exon 2), Nijmegen (FGB, c.220C>T), Naples (FGB, c.292G>A), and Melun (FGG, c.1169A>T) have been related to an increased risk of thrombosis [5].
The overall prevalence of afibrinogenemia has been estimated at 1 in 1,000,000 people, but it is assumed to be higher where consanguineous marriage is practiced. Hypofibrinogenemia and dysfibrinogenemia are more common but tend to remain undetected, so precise data regarding their epidemiology cannot be provided. About 500 cases of dysfibrinogenemia have been reported since the first description of the disease in 1958 [4]. Males and females are affected equally by CFD [2].
The conversion of fibrinogen to cross-linked fibrin is the concluding step in the final common pathway of coagulation. It's a prerequisite for the formation of a stable thrombus and the culmination of what is referred to as secondary hemostasis. This is by far the most widely known function of fibrinogen, but it is not the only one. Fibrinogen is also involved in primary hemostasis, due to its ability to form bridges between activated thrombocytes. This way, fibrinogen facilitates the formation of a primary platelet plug [4]. The complete absence of fibrinogen thus causes severe hemophilia by impeding the aggregation of platelets and by interrupting the coagulation cascade, regardless of its intrinsic or extrinsic activation.
Different mechanisms may underly the prothrombotic activity of abnormal fibrinogen. Under physiological conditions, fibrin limits by binding thrombin, its major activator, in a sort of negative-feedback loop. If this regulatory mechanism doesn't work, patients may become prone to thrombosis. This is commonly observed in certain types of dysfibrinogenemia, but, surprisingly, has also been postulated as a possible cause of thrombotic complications in quantitative CFD [4]. Besides dysfunctional feedback mechanisms, the risk of thrombotic complications may be increased by abnormal fibrinogen impairing fibrinolysis [5].
Affected families may benefit from genetic counseling. The prenatal diagnosis of CFD is feasible and should be established if the family harbors a pathogenic mutation causing afibrinogenemia [4]. Hypofibrinogenemia and dysfibrinogenemia are unlikely to interfere with prenatal development so that the corresponding studies can be postponed until after birth.
Prophylaxis of hemorrhages should be considered in all cases of afibrinogenemia and may be offered from birth [2]. Due to the long half-life of fibrinogen, weekly or biweekly applications of fibrinogen concentrates suffice to maintain plasma levels between 0.5 and 1.0 g/l. Further increases in the concentration of fibrinogen are associated with high risks of thrombotic complications and should be avoided.
CFD is a general term referring to any quantitative or qualitative deficiency of fibrinogen, the most abundant clotting factor in the human circulation. Three major types of CFD should be distinguished [2]:
Afibrinogenemia, a complete lack of fibrinogen
Hypofibrinogenemia, associated with plasma levels of fibrinogen <1.5 g/l
Dysfibrinogenemia, where abnormal fibrinogen is circulating that may hinder or favor the formation of blood clots
In literature, afibrinogenemia and hypofibrinogenemia, both variants of quantitative CFD, may also be referred to as CFD type 1, whereas CFD type 2 stands for qualitative deficiencies of fibrinogen [4]. Notwithstanding the utility of these classification systems, the genetic and clinical aspects of CFD are more complex. This particularly applies to dysfibrinogenemia, since the abnormal structure of fibrinogen may interfere with the formation of thrombi or promote blood clotting. Thus, affected individuals may present with a hemorrhagic diathesis or a tendency to thrombosis.
This article aims at summarizing the features of all types of CFD, but the interested reader is strongly encouraged to revise the specific contents on this platform that treat with congenital afibrinogenemia, congenital hypofibrinogenemia, and hereditary dysfibrinogenemia.
Hereditary fibrinogen Aα chain amyloidosis will not be discussed in this article, but excellent literature on this topic is available elsewhere [9] [10].
Congenital fibrinogen deficiency (CFD) is a rare, hereditary bleeding disorder. Distinct mutations of the genes encoding for fibrinogen may interrupt the synthesis of this clotting factor o may result in the production of dysfunctional fibrinogen. Accordingly, afibrinogenemia (no fibrinogen at all), hypofibrinogenemia (reduced amounts of functional fibrinogen), and dysfibrinogenemia (formation of abnormal fibrinogen) are distinguished. But how does fibrinogen affect the balance between procoagulant and anticoagulant reactions?
Under physiological conditions, fibrinogen is converted to fibrin in the final step of the coagulation cascade. Cross-linked fibrin constitutes the matrix of stable blood clots. Thus, in the absence of fibrinogen, durable thrombi cannot be formed, and the patient becomes prone to hemorrhages. This condition is present at birth, and severe cases manifest in umbilical cord bleeding, mucosal hemorrhages, hematoma formation, or bleeding into joint spaces within the neonatal period. Patients with mild to moderate CFD tend to remain asymptomatic until they sustain traumatic injuries, or, with regard to women, until they reach the fertile age. Female CFD patients often describe prolonged, heavy menstrual flows, and they may suffer recurrent losses of pregnancy.
Somewhat surprisingly, certain types of CFD manifest in an increased risk of thrombosis and thromboembolism. This may happen if abnormal fibrinogen is produced that favors the formation of blood clots.
Treatment of hemorrhagic CFD mainly consists in replacing fibrinogen. However, this type of therapy bears the risk of an overcompensation, thereby predisposing the patient to thrombotic disease. Thrombosis, in turn, is treated with anticoagulants that counteract fibrinogen. To maintain the delicate equilibrium between both extremes of the coagulation system, each therapy needs to be adjusted to the patient's individual needs. In cases of mild or moderate CFD, it is best maintained by the body itself, and treatment isn't required unless the patient becomes symptomatic, pregnant, or is about to undergo surgery. Permanent therapy is recommended in case of severe CFD to prevent life-threatening vascular accidents.
Palla R, Peyvandi F, Shapiro AD. Rare bleeding disorders: diagnosis and treatment. Blood. 2015; 125(13):2052-2061.
Peyvandi F. Epidemiology and treatment of congenital fibrinogen deficiency. Thromb Res. 2012; 130 Suppl 2:S7-11.
Tziomalos K, Vakalopoulou S, Perifanis V, Garipidou V. Treatment of congenital fibrinogen deficiency: overview and recent findings. Vasc Health Risk Manag. 2009; 5:843-848.
de Moerloose P, Casini A, Neerman-Arbez M. Congenital fibrinogen disorders: an update. Semin Thromb Hemost. 2013; 39(6):585-595.
Casini A, Neerman-Arbez M, Ariëns RA, de Moerloose P. Dysfibrinogenemia: from molecular anomalies to clinical manifestations and management. J Thromb Haemost. 2015; 13(6):909-919.
Margaglione M, Vecchione G, Cappucci F, et al. Venous thrombosis in afibrinogenemia: a successful use of rivaroxaban. Haemophilia. 2015; 21(5):e431-433.
Roqué H, Stephenson C, Lee MJ, et al. Pregnancy-related thrombosis in a woman with congenital afibrinogenemia: a report of two successful pregnancies. Am J Hematol. 2004; 76(3):267-270.
Sartori MT, Milan M, de Bon E, Fadin M, Pesavento R, Zanon E. Thrombosis of abdominal aorta in congenital afibrinogenemia: case report and review of literature. Haemophilia. 2015; 21(1):88-94.
Stangou AJ, Banner NR, Hendry BM, et al. Hereditary fibrinogen Aα-chain amyloidosis: phenotypic characterization of a systemic disease and the role of liver transplantation. Blood. 2010; 115(15):2998-3007.
Yazaki M, Yoshinaga T, Sekijima Y, Kametani F, Okumura N. Hereditary Fibrinogen Aα-Chain Amyloidosis in Asia: Clinical and Molecular Characteristics. Int J Mol Sci. 2018; 19(1).

redpajama_set_name: RedPajamaCommonCrawl


I've always cooked all my girls' meals. I think there's nothing better for them than home-cooked meals using the freshest ingredients I can buy. Baby food is often heat-treated to ensure it has a long shelf life, but it's heated to such a degree that I wonder if any nutrients are left in the vegetables at all after that process? I absolutely do not judge any parent who uses these meals: they're convenient and are food for babies after all. They're just not for me.
However, preparing and cooking yummy, nutritious meals day after day can become exhausting for even the most enthusiastic cook.
Cooking for you and your partner is one thing, but once baby comes along and starts eating food at around 4-6 months you suddenly have a LOT more cooking to do. Then you might have another baby, and you're making meal after meal every day. (Sometimes multiple dishes at each meal time if you're dealing with a fussy eater, allergies, food intolerance and so on.) Grocery shopping, meal planning, slicing, chopping, cutting, boiling, steaming, pureeing… it's a lot of work!
But 'til recently, there's been little alternative if you want organic home-cooked meals for your baby or toddler.
I first read about Baby Bistro on Rebecca Judd Loves blog and have been so keen to try them myself to see just how fresh and delicious they were. I haven't felt the need to buy them until my third baby started eating solids recently, and believe me, the meal preparation in my house went through the roof!
Baby Bistro offers healthy, nutritious baby and toddler meals that are prepared and cooked right here in Melbourne. They have some stockists, but more impressively, they deliver them to your home – frozen, and packed in portion-sized containers. Super easy to store and even easier to serve.
All the ingredients are simple so are appealing to kids, and the meals are made with healthy, organic food that is cooked, packaged then frozen. Just like I do at home!
And I couldn't agree more.
Some of the meals are amazing – like red lentils with vegetables, cheesy fish with broccoli and cauliflower and vegetable ratatouille. Perfect, because I hate cooking fish! New tastes and flavours are great for my girls. Encourages them to try new foods and not get too fussy.
It's such a great idea for busy mums, working parents – or those that don't like cooking – who often don't have time to cook fresh, nutritious meals all the time. You can just order the meals online and they deliver them to your door.


Described in detail is how to work safely with difficult to machine and exotic materials on a metal lathe and benchtop mill. In addition, a section about cutting tools and materials properties is included. Textboxes explain the chemistry, material science, and nanoscience background - in plain English.
The (6"x9") paperback print has 128 pages, 60 figures, 15 info text boxes, and 2 tables as well as a detailed index and contents list for easy reference.
The described work is doable on any lathe/mill.
Materials discussed: Alloy Steel, Aluminum, Bronze, Brass, Solid Carbide, Cast Iron, Steel, Ceramics – Macor, Cork, Copper, Free Machining Materials, Pure Manganese, Magnets (Superalloys), Plastics, Rocks, Sandwich Structures – Hardened Steel, HSS, cutting High Speed Steel, Stainless Steel, Styrofoam, Sterling Silver, Tool Steel, Ledloy, Titanium, Wax, and Wood Convince your wife/friend about spending thousands a year on greasy equipment: make her/him a pair of earrings cut from Sterling Silver or Titanium or machine your own solid carbide tools. How that can be done is described here. The author is a physical-chemistry college teacher and hobby machinist. This booklet of the LatheCity book series is written for more advanced homeshop machinists.


In 1929 the California Self-Insurers Association came into being. Its stated purpose was to monitor and protect the legitimate interests of self-insurers in the workers' compensation field. The California Self-Insurers Association performs these functions by providing educational opportunities as well as legislative and regulatory support and analysis to its members.
Today CSIA has over 100 members, representing many of California's largest companies. The association provides ongoing representation and leadership in the field of self-insured workers' compensation issues. Members benefit from the valuable resources, ongoing educational programs and two annual conferences put on by the association.
Joining CSIA helps California businesses who choose to self insure their workers' compensation liabilities create a united voice in the complicated and often contentious subject. If you are not a member, please consider joining us and help California businesses lead the Golden State back into economic prosperity. A membership application is available in the Membership section of this website.
CSIA's mission is to champion and promote the interests of self-insured employers in California by providing leadership on workers' compensation matters.
CSIA is THE trusted voice for California self-insured employers and their employees.


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How this Indianapolis native outed Mark Felt as Watergate's 'Deep Throat'
Attorney John O'Connor says he met the tipster's grandson by happenstance during a dinner party.
How this Indianapolis native outed Mark Felt as Watergate's 'Deep Throat' Attorney John O'Connor says he met the tipster's grandson by happenstance during a dinner party. Check out this story on IndyStar.com: http://indy.st/2zHRTym
Holly V. Hays, holly.hays@indystar.com Published 6:53 p.m. ET Oct. 26, 2017 | Updated 7:55 p.m. ET Oct. 27, 2017
For years, we only knew him as 'Deep Throat,' but Mark Felt is "the man who brought down the White House." Now Liam Neeson is bringing Felt's side of the Nixon Watergate scandal to the big screen. USA TODAY
Indianapolis native John O'Connor (left) identified Mark Felt (right) as Watergate's "Deep Throat" in a 2005 Vanity Fair article and later wrote a book about Felt that inspired a major motion picture.(Photo: Provided by John O'Connor)
Decades before Donald Trump fired off tweets about FBI leaks, a senior intelligence official huddled with a Washington Postreporter in a dark, damp parking garage and fed him breadcrumbs along a trail that would end in a president's resignation.
W. Mark Felt was the second in command at the FBI at the time it was investigating President Richard Nixon and his men in the months following a June 1972 break-in at the Democratic National Committee headquarters in the Watergate business complex in Washington, D.C. The cover-up of a host of legally questionable activities would eventually result in Nixon's ouster in August 1974.
During that time, Felt "wrote the book" on leaking, San Francisco-based attorney John O'Connor said.
O'Connor, a 70-year-old native of Indianapolis' north side, outed Felt to the world as Watergate's "Deep Throat" in a July 2005 article for Vanity Fair. Now, Felt's biography has become a major motion picture.
"Mark Felt: The Man Who Brought Down the White House" is set to hit Indianapolis-area theaters Friday and stars Liam Neeson in the title role.
Felt "knew, deep down inside, that what he did was right," O'Connor told IndyStar.
'Deep Throat' theories
Post reporters Bob Woodward and Carl Bernstein introduced readers to "Deep Throat" in the 1974 narrative "All the President's Men," which details their investigation from the day of the break-in through January 1974, months before Nixon's resignation. They described the informant as a source with an "extremely sensitive" position within the executive branch with whom Woodward conducted secret meetings in the middle of the night. Hal Holbrook portrayed "Deep Throat" in the 1976 film.
For years, theories circulated about who the informant could have been. The reporters — and the Post — swore to protect his identity, and O'Connor thinks Felt would have been happy never to have revealed his secret.
"Had Woodward not featured this character in the book ... no one ever would've known that he leaked," O'Connor said. "He would've gone to the grave with that."
Mark Felt appeared on CBS' "Face The Nation" on Aug. 30, 1976. (Photo: Associated Press)
O'Connor said he had known since the 1970s that Felt was the man behind "Deep Throat" — "that was a real obsession of mine," he said — but he didn't get the chance to confirm it until he met Felt's grandson by happenstance at a dinner party O'Connor and his wife threw for their daughter and some friends in 2002.
O'Connor was telling stories of his own father's days with the FBI when one of his daughter's friends spoke up.
"I was just telling some funny stories when the young fellow across the table from me said, 'Well, maybe your father knew my grandfather. He was in the FBI. … His name's Mark Felt,'" O'Connor remembered. "My jaw dropped."
Outed in Vanity Fair
Through the grandson he met Felt. It took three years for O'Connor to persuade him — and a publication — that it was time to bring "Deep Throat" out of the shadows. Although O'Connor said Felt knew he did the right thing, he was afraid of the repercussions it would have for the Bureau.
"He always felt that some of the power of the FBI was its reputation, was of the conduct of its agents," O'Connor said. "He knew that this culture that he was in charge of — he was in charge of the culture for many years — that it was a very strict, strict, no-nonsense culture, that those guys may not understand."
Working as the family's attorney, O'Connor was finally able to convince Vanity Fair that their story was credible and that Felt was ready to come forward. The story published in May 2005 and was featured in the magazine's July issue.
After the Vanity Fair article, Woodward, Bernstein and the Post confirmed Felt's identity. Two months later, in July 2005, Woodward published "The Secret Man," which detailed the relationship between the top FBI official and the investigative reporter.
From left: Former Washington Post reporter Carl Bernstein, attorney John O'Connor, Mark Felt and Washington Post associate editor Bob Woodward pose in an undated photo after Felt's identity as "Deep Throat" was revealed. (Photo: Provided by John O'Connor)
"'Secret Man' was not especially kind to him," O'Connor said. "'All the President's Men' was much kinder to 'Deep Throat' and in my view much more truthful because there was no need to take gratuitous shots at the FBI."
When he came out, Felt was criticized by some, including those at the FBI, for being the agent who undermined the Nixon presidency. But there were others, like O'Connor, who lauded him for being a hero who stood up for what was right.
"He was not trying to get the president," O'Connor said. "He was not trying to get (FBI Acting Director L. Patrick) Gray. He was just trying to do his job, but they kept making the mistake of trying to stop him. And unfortunately he's not a guy that would just shut up and go along with it.
"There's no doubt he was taking big chances."
Speaking out put Felt's inner turmoil to rest.
"He was in a prison that he made himself," O'Connor said, "and I think we helped him get out of prison."
Coming out of the shadows lifted the weight off Felt's shoulders in his final years, O'Connor said. Felt died Dec. 18, 2008, at age 95, just over three years after the big reveal. O'Connor thinks the new film is a perfect ending to the story that started with "All the President's Men."
The film depicts the internal hunt among Washington officials to determine the identity of the well-placed whistleblower and shows the tensions between the executive and judicial branches.
The story, though decades old, feels relevant in 2017's political climate. Just months ago, Trump publicly accused former FBI Director James Comey of leaking classified information to reporters. O'Connor said he believes there will always be a place for leakers in the American governmental system.
That's not to say the White House should be a sieve. O'Connor said he thinks there should probably be more punitive action taken against leakers who divulge information that could damage national security — something Felt was careful never to do. But ethical whistleblowers, O'Connor said, are the people you hope will stand up in risky situations.
"If you leak for purposes of upholding ethical standards, of making sure that your government or corporation does not break a law or do something unethical, I think that's really the power of our democracy," O'Connor said. "I think that's where democratic systems heal themselves."
Call IndyStar reporter Holly Hays at (317) 444-6156. Follow her on Twitter: @hollyvhays.
Read or Share this story: http://indy.st/2zHRTym
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