Elizabeth M Angus’s research while affiliated with University Hospital Southampton NHS Foundation Trust and other places

Corrigenda to the abovementioned paper are given, as well as new data on Aphodius (Liothorax) felix Angus et al., 2024 and A. (L.) bellumgerens Angus et al., 2024

The Palaearctic species of Aphodius Hellwig, 1798, subgenus Liothorax Motschulsky, 1860 are revised using a combination of chromosome analysis, molecular phyloge-netics and morphological statistical analysis. Sixteen species are recognised, one of which is shown to comprise two subspecies. Based mainly on the morphology of the aedeagal endophallus and the phylogenetic analysis, they are placed in two groups: the. niger group, apparently monophyletic, comprising Aphodius (Liothorax) niger Illig-er, 1798, A. (L.) muscorum (Ádám, 1994), stat. rest., A. (L.) felix sp. nov., A. (L.) bel-lumgerens sp. nov., A. (L.) bameuli sp. nov., A. (L.) krelli sp. nov., A. (L.) isikdagensis (Balthasar, 1953), A. (L.) alberti sp. nov. and A. (L.) wilsonae Maté et Angus, 2005, stat. rest.; and the plagiatus group, almost certainly paraphyletic, comprising A. (L.) plagiatus (Linnaeus, 1767), including A. (L.) p. plagiatus and A. (L.) p. sinoplagiatus subsp. nov., A. (L.) rodrigoi sp. nov., A. (L.) discoides A. Schmidt, 1916, stat. rest., A. (L.) rutilipennis (Baudi di Selve, 1870), stat. rest., A. (L.) chellala sp. nov., A. (L.) kraatzi Harold, 1868, and A. (L.) rusakovi Gusakov, 2004. A key to the species is given as well as details of their morphology, distributions, and habitats.

The Palaearctic species of Aphodius Hellwig, 1798, subgenus Liothorax Motschulsky, 1860 are revised using a combination of chromosome analysis, molecular phyloge-netics and morphological statistical analysis. Sixteen species are recognised, one of which is shown to comprise two subspecies. Based mainly on the morphology of the aedeagal endophallus and the phylogenetic analysis, they are placed in two groups: the. niger group, apparently monophyletic, comprising Aphodius (Liothorax) niger Illig-er, 1798, A. (L.) muscorum (Ádám, 1994), stat. rest., A. (L.) felix sp. nov., A. (L.) bel-lumgerens sp. nov., A. (L.) bameuli sp. nov., A. (L.) krelli sp. nov., A. (L.) isikdagensis (Balthasar, 1953), A. (L.) alberti sp. nov. and A. (L.) wilsonae Maté et Angus, 2005, stat. rest.; and the plagiatus group, almost certainly paraphyletic, comprising A. (L.) plagiatus (Linnaeus, 1767), including A. (L.) p. plagiatus and A. (L.) p. sinoplagiatus subsp. nov., A. (L.) rodrigoi sp. nov., A. (L.) discoides A. Schmidt, 1916, stat. rest., A. (L.) rutilipennis (Baudi di Selve, 1870), stat. rest., A. (L.) chellala sp. nov., A. (L.) kraatzi Harold, 1868, and A. (L.) rusakovi Gusakov, 2004. A key to the species is given as well as details of their morphology, distributions, and habitats.

The Palaearctic species of Aphodius Hellwig, 1798, subgenus Liothorax Motschulsky, 1860 are revised using a combination of chromosome analysis, molecular phylogenetics and morphological statistical analysis. Sixteen species are recognised, one of which is shown to comprise two subspecies. Based mainly on the morphology of the aedeagal endophallus and the phylogenetic analysis, they are placed in two groups: the. niger group, apparently monophyletic, comprising Aphodius (Liothorax) niger Illiger, 1798, A. (L.) muscorum (Ádám, 1994), stat. rest., A. (L.) felixsp. nov., A. (L.) bellumgerenssp. nov., A. (L.) bameulisp. nov., A. (L.) krellisp. nov., A. (L.) isikdagensis (Balthasar, 1953), A. (L.) albertisp. nov. and A. (L.) wilsonae Maté et Angus, 2005, stat. rest.; and the plagiatus group, almost certainly paraphyletic, comprising A. (L.) plagiatus (Linnaeus, 1767), including A. (L.) p. plagiatus and A. (L.) p. sinoplagiatussubsp. nov., A. (L.) rodrigoisp. nov., A. (L.) discoidesA. Schmidt, 1916, stat. rest., A. (L.) rutilipennis (Baudi di Selve, 1870), stat. rest., A. (L.) chellalasp. nov., A. (L.) kraatzi Harold, 1868, and A. (L.) rusakovi Gusakov, 2004. A key to the species is given as well as details of their morphology, distributions, and habitats.

Helophorus cincticollis Guillebeau, 1893 is confirmed as a European species as a result of recent discoveries in the spanish province of Cadiz.

A lectotype is designated for the Tibetan species Deronectesemmerichi Falkenström, 1936 (Currently Boreonectesemmerichi (Falkenström)), and its habitus, as well as the median lobe and parameres of its aedeagus, are figured along with additional comparative material. Material of Boreonectesemmerichi from Sikkim (BMNH) represents the first record of a Boreonectes Angus, 2010 species from India. The karyotype of Boreonectesemmerichi is described as having 26 pairs of autosomes plus sex chromosomes which are X0 (♂), XX (♀). The karyotype is most like that of Boreonectesmacedonicus (Géuorguiev, 1959), but with slight differences. Additional chromosomal information is given for Boreonectesgriseostriatusgriseostriatus (De Geer, 1774) in the French Alps, Boreonectesgriseostriatusstrandi (Brinck, 1943) on the Kola Peninsula, Boreonectesmultilineatus (Falkenström, 1922) in the Pyrenees and Boreonectesibericus (Dutton & Angus, 2007) in the Spanish Picos de Europa.

Summary A girl aged 6 presented with haematuria and her sister (aged 5) presented with haematuria and proteinuria. Family history showed multiple individuals suffering from end stage renal failure from the paternal side of the pedigree. Following kidney biopsy in the father and paternal grandmother, the pathological diagnosis was of focal segmental glomerulosclerosis (FSGS). Exome sequencing was undertaken in the proband's sister and grandmother. Genetic variants shared by both affected individuals were interrogated to identify the genetic cause of disease. Candidate variants were then sequenced in all the family members to determine segregation with the disease. A mutation of COL4A5 known to cause Alport syndrome segregated with disease from the paternal side of the pedigree and a variant in NPHS1 was present in both paediatric cases and inherited from their mother. This study highlights the advantages of exome sequencing over single gene testing; disease presentation can be heterogeneous with several genes representing plausible candidates; candidate gene(s) may be unavailable as a diagnostic test; consecutive, single gene testing typically concludes once a single causal mutation is identified. In this family, we were able to confirm a diagnosis of Alport syndrome, which will facilitate testing in other family members.

A 2-year-old patient with a neuroblastoma developed haemolytic uraemic syndrome (HUS) following treatment with cisplatin and carboplatin. Following treatment with eculizumab, there was a substantial improvement in renal function with the recovery of the platelet count and the cessation of haemolysis. Subsequent investigations showed a novel, heterozygous CD46 splice site mutation with reduced peripheral blood neutrophil CD46 expression. Withdrawal of eculizumab was followed by the recurrence of disease activity, which resolved with re-introduction of therapy. Abnormal regulation of complement may be associated with other cases of cisplatin-induced HUS and treatment with eculizumab may be appropriate for other affected individuals.

Background: Atypical haemolytic uraemic syndrome (aHUS) is caused by dysregulated complement activation. A humanised anti-C5 monoclonal antibody has recently become available for treatment of this condition Case-diagnosis/treatment: We present the first description of an infant with an activating mutation of complement factor B successfully treated with eculizumab. On standard doses she had evidence of ongoing C5 cleavage despite a good clinical response. Conclusions: Eculizumab is effective therapy for aHUS associated with factor B mutations, but recommended doses may not be adequate for all patients.