Macrotristria monteithi sp. n., a large new cicada from central Queensland with a small distribution (Cicadoidea, Cicadidae, Macrotristriini).

A new species of cicada, Macrotristria monteithi sp. n., is described from the southern Carnarvon and Expedition Ranges in central Queensland, Australia. It is a large species allied to the common and widespread species M. angularis, but unlike that species it has a comparatively narrow distribution.

An impressive new species of mugadina from queensland with notes on a congeneric species (cicadidae: cicadettinae: cicadettini).

This contribution details the morphology, distribution, and song characteristics of a new grass cicada species within the genus Mugadina Moulds, 2012, previously represented by only two much smaller species. The new species is M. superba sp. n. It occurs widely in central Queensland, occurring in a broad curved zone between the western desert areas and the eastern coast. Details of the morphology and the ticking calling songs presented are given, and detailed comparisons are made of morphology and songs between M. superba sp. n. and M. marshalli (Distant, 1911).

A revision of the Australian cicada genus Punia Moulds, 2012 (Cicadidae: Cicadettinae: Cicadettini) with the description of four new species.

Punia minima (Goding Froggatt, 1904) from the Northern Territory is redescribed and the female described for the first time. Four new species found across the monsoonal north of Australia are documented: P. hyas sp.n., P. limpida sp.n., P. kolos sp.n. and P. queenslandica sp.n. A key to all five species is provided and their phylogenetic relationships discussed.

Cicada fossils (Cicadoidea: Tettigarctidae and Cicadidae) with a review of the named fossilised Cicadidae.

The Cicadoidea comprise two families, the Cicadidae and the Tettigarctidae. This paper evaluates the status and taxonomy of all named Cicadoidea fossils belonging to the Cicadidae. Shcherbakov (2009) has previously revised the Tettigarctidae. Two new genera are described, Camuracicada gen. n. and Paleopsalta gen. n., for Camuracicada aichhorni (Heer, 1853) comb. n. and Paleopsalta ungeri (Heer, 1853) comb. n. A lectotype is designated for Cicada emathion Heer, 1853.          Cicada grandiosa Scudder, 1892 is transferred to Hadoa Moulds, 2015 as Hadoa grandiosa comb. n.; Oncotympana lapidescens J. Zhang, 1989 is transferred to Hyalessa China, 1925 as Hyalessa lapidescens comb. n.; Meimuna incasa J. Zhang, Sun X. Zhang, 1994 and Meimuna miocenica J. Zhang X. Zhang, 1990 are transferred to Cryptotympana Stål, 1861 as Cryptotympana incasa comb. n. and Cryptotympana miocenica comb. n.; Tibicen sp. aff. japonicus Kato, 1925 is transferred to Auritibicen as Auritibicen sp. aff. japonicus comb. n., and Terpnosia sp. aff. vacua Olivier, 1790 is transferred to Yezoterpnosia Matsumura, 1917 as Yezoterpnosia sp. aff. vacua comb. n. The generic placement of two other fossils is changed to reflect current classification, those species now being Auritibicen bihamatus (Motschulsky, 1861) and Yezoterpnosia nigricosta (Motschulsky, 1866).         Two species, Davispia bearcreekensis Cooper, 1941 and Lithocicada perita Cockerell, 1906, are transferred from the subfamily Cicadinae to the Tibicininae, tribe Tibicinini. Cicadatra serresi (Meunier, 1915) is also transferred from the Cicadinae to the Cicadettinae because the Cicadatrini have recently been transferred from the Cicadinae to the Cicadettinae (Marshall et al. 2018).         Miocenoprasia grasseti Boulard and Riou, 1999 is transferred from the tribe Prasiini to the Lamotialnini. Tymocicada gorbunovi Becker-Migdisova, 1954 is transferred from the Dundubiini to the Cryptotympanini; Paracicadetta oligocenica Boulard Nel, 1990 is transferred from the Cicadettini to the Pagiphorini and Minyscapheus dominicanus Poinar et al., 2011 is assigned to the Taphurini. Names of species once considered to belong in Cicadidae, but now excluded, are listed with explanation.

Contextual representations of negative images modulate intrusion frequency in an intrusion provocation paradigm.

BACKGROUND AND OBJECTIVES: To understand how memories of negative events become highly accessible in the context of trauma, we tested the hypothesis that contextual information modulates how easily intrusions can be provoked by perceptual stimuli.. METHODS: Healthy participants viewed pictures depicting trauma scenes either with or without accompanying moderate (i.e. survival, recovery) or severe (i.e. fatality, permanent injury) outcome information. All participants viewed the same depictions of trauma scenes. Involuntary memories for the pictures were assessed using self-report diaries and an adapted version of the Impact of Event Scales (IES). A blurred picture perceptual priming paradigm was adapted to be used as an intrusion provocation task. RESULTS: The severe outcome group experienced a significantly higher frequency of intrusions on the intrusion provocation task in comparison to both moderate outcome and control (no-context) conditions. The severe outcome condition did not increase intrusions on the self-report diaries or the adapted IES. There was no effect of condition on ratings for the emotionality, self-relevance, valence, or seriousness of the trauma scenes. LIMITATIONS: The analogue method should not be generalized directly to incidences of real-life trauma. It was unclear why differences in intrusion frequency were found in the provocation task only. The relative amount of individual conceptual and data-driven processing adopted by the participants was not assessed. CONCLUSIONS: Manipulating contextual information that determines the meaning of sensory-perceptual features for a trauma scene can modulate subsequent intrusion frequency in response to visually similar cues.

Determination of optimal method for antibody identification in a reference laboratory.

Methods commonly used for antibody identification are hemagglutination (tube), column agglutination (gel), and solid-phase red cell adherence. Our AABB immunohematology reference laboratory (IRL) conducted a study to determine which antibody identification testing method was optimal for detecting all clinically significant antibodies. Patient specimens were sent to our IRL from August 2008 to September 2009. Routine testing was performed by tube method and then by manual gel and manual solid-phase methods. Of the 254 samples tested, 115 showed agreement in antibody identification with all three methods. The tube method identified all but six clinically significant antibodies. The gel method did not identify 59 clinically significant antibodies. Fifty-six clinically significant antibodies were not identified by solid-phase testing. Tube testing identified 27 clinically insignificant antibodies, primarily cold autoantibodies. Gel and solid-phase methodologies identified two and three cold autoantibodies, respectively. Solid-phase testing failed to detect 12 examples of anti-K. No identifiable pattern of reactivity was found in 13 samples using gel testing compared with 6 for solid-phase and none for tube methodologies. Hemagglutination tube method was the best choice for our IRL because it missed the fewest number of clinically significant alloantibodies. Benefits also included the ability to use various potentiating factors, incubation times, and temperature phases to enhance antibody identification. The tube method provided critical data for determining antibody clinical significance.

Revealing negative thinking in recovered major depression: a preliminary investigation.

Previous research suggests that formerly dysphoric individuals engage in effortful strategies (e.g., thought suppression) that may mask underlying depressive thinking. The addition of a cognitive load, such as recalling a 6-digit number, which interferes with effortful mental control, reveals depressive thinking in formerly dysphoric individuals. This preliminary study tested whether this effect of cognitive load on revealing negative thinking generalizes to formerly clinically depressed patients. Currently depressed patients, recovered depressed patients and never-depressed patients unscrambled sentences that could form either positive or negative statements, after random allocation to either cognitive load or no cognitive load conditions. The number of negative statements unscrambled was used as an index of negative thinking. Without a load, recovered depressed patients did not differ from never-depressed controls: both groups completed fewer negative statements than currently depressed patients. However, the cognitive load increased negative statements in the recovered depressed group, making them resemble the currently depressed group more than the never-depressed group. These preliminary findings extend previous demonstrations of cognitive load unmasking negative thinking in dysphoric students to a clinical population, suggesting that formerly depressed patients utilize effortful strategies to minimize the report of negative thinking, which is undermined by the addition of a cognitive load.

The Redelberger antigen: a family study, a family story.

The Redelberger antigen (Rba) was first discovered in 1974 on the RBCs of a blood donor who was an employee of the Community Blood Center in Dayton, Ohio. The discovery was made as a result of the investigation of a reagent contamination problem. Two examples of the Rba antigen were subsequently identified in the United Kingdom,but no "new"examples have been identified in the United States or Europe. Anti-Rba is a commonly occurring antibody, often found in combination with other antibody specificities, especially in combination with other antibodies to low-incidence antigens.

Review: monoclonal reagents and detection of unusual or rare phenotypes or antibodies.

Monoclonal antibodies have been used in the formulation of commercially available blood grouping reagents since the early 1990s. It became apparent early on that introducing them into routine use along with, or instead of, human- or animal-derived reagents could and did lead to discrepant reactions. These discrepancies most often came to light when confirming a blood type obtained previously with human- or animal-source reagents or when using two or more sources of a reagent from the same or another manufacturer to perform blood typing or antibody detection or identification testing. A number of factors contribute to differences in reactivity of reagents that are of the same specificity but are from more than one source. One factor is the use of different clones of the same specificity to manufacture blood bank reagents. Another is the effect of the various diluents used by different manufacturers to formulate reagents that contain the same clone(s). In addition, RBCs having unusual or rare phenotypes can cause discrepant reactions when performing phenotyping. Discrepant reactions can also occur because of patient or donor antibodies that react in an unusual manner when antiglobulin tests are performed with monoclonal antihuman globulin (AHG) versus rabbit AHG reagent. It is important to know the identity of the unusual or rare phenotypes and antibodies and to be able to recognize the different types of reactions that will be observed when using more than one reagent of the same specificity. Most importantly, one must be able to interpret reactions correctly and establish the true blood type of the RBCs or specificity of the antibodies. This review will describe situations in which the use of monoclonal reagents from more than one source or manufacturer, or comparison with results of human- and animal-source reagents, resulted in discrepancies with unusual or rare phenotypes or antibodies. Many of the samples described in this review were sent to the reference laboratory at Gamma Biologicals, Inc., in Houston, Texas, which later became ImmucorGamma with sites in Norcross, Georgia, and Houston, Texas.

Case report:DNA testing resolves unusual results in the Dombrock system.

Typing for antigens in the Dombrock blood group system and identifying the corresponding antibodies are notoriously difficult tasks. The reagents are scarce and the antibodies are weakly reactive. When RBCs from family members of a patient with an antibody to a high-prevalence Dombrock antigen were tested for compatibility,an unusual pattern of inheritance was observed:RBCs from the patient's children and one niece, in addition to those from some of the patient's siblings,were compatible. This prompted the performance of DNA-based assays for DO alleles and the results obtained were consistent with and explained the compatibility test results. It was possible to study this large kindred because of the cooperation of family members, hospital personnel, and reference laboratory staff.

Reactivity of FDA-approved anti-D reagents with partial D red blood cells.

Individuals whose RBCs are characterized as having a partial D phenotype may make anti-D if exposed to normal D+ RBCs; thus it is desirable that they be typed as D- should they require blood transfusion or Rh immune globulin (RhIG) prophylaxis. Further, use of different anti-D reagents by blood centers and transfusion services can account for FDA-reportable errors. For this study, anti- D reagents for use in tube tests were obtained from three U.S. manufacturers. They included three examples of IgM monoclonal anti-D blended with monoclonal IgG anti-D, one IgM monoclonal anti-D blended with polyclonal IgG anti-D, and two reagents formulated with human anti-D in a high-protein diluent. One anti- D formulated for use by gel column technology was also tested. Direct agglutination tests by tube or gel were strongly positive (scores 9-12), with partial D RBCs of types DII, DIIIa, DIIIb, and DIVa. No reagent anti-D caused direct agglutination of DVI type 1, DVI type 2, or DFR phenotype RBCs. One tube anti-D reagent formulated with an IgM monoclonal anti-D plus a polyclonal IgG anti-D failed to cause direct agglutination of DVa, DBT, and R(0)(Har) RBCs, while DVa RBCs reacted weakly with two high-protein reagents formulated with human IgG anti-D. In contrast, the anti-D used by gel column technology was strongly reactive (score 11) with DVa, DBT, and R(0)(Har) RBCs. The single monoclonal IgM-polyclonal IgG blended anti-D and the two high-protein reagents were also the only reagents that failed to react with R(0)(Har) RBCs by the IAT. Elimination of the test for weak D on all patient samples, using currently available FDA-licensed reagents, will ensure that partial D category VI (DVI) patients will type as D- for the purpose of RhIG prophylaxis and blood transfusion. However, RBCs of other partial D phenotypes will be classified as D+ in direct agglutination tests with some, if not all, currently available reagents. Testing donors for weak expression of D continues to be required, albeit that Rh alloimmunization by RBCs with a weak or partial D phenotype is uncommon. Further, because of differences in performance characteristics among FDA-approved reagents, conflicts between donor center D typing and transfusion service confirmatory test results are inevitable.

Genomic analysis of clinical samples with serologic ABO blood grouping discrepancies: identification of 15 novel A and B subgroup alleles.

Since the cloning in 1990 of complementary DNA corresponding to messenger RNA transcribed at the blood group ABO locus, polymorphisms and phenotype-genotype correlations have been reported by several investigators. Exons 6 and 7, constituting 77% of the gene, have been analyzed previously in samples with variant phenotypes but for many subgroups the molecular basis remains unknown. This study analyzed 324 blood samples involved in ABO grouping discrepancies and determined their ABO genotype. Samples from individuals found to have known subgroup alleles (n = 53), acquired ABO phenotypes associated with different medical conditions (n = 65), probable chimerism (n = 3), and common red blood cell phenotypes (n = 109) were evaluated by ABO genotype screening only. Other samples (n = 94) from apparently healthy donors with weak expression of A or B antigens were considered potential subgroup samples without known molecular background. The full coding region (exons 1-7) and 2 proposed regulatory regions of the ABO gene were sequenced in selected A (n = 22) or B (n = 12) subgroup samples. Fifteen novel ABO subgroup alleles were identified, 2 of which are the first examples of mutations outside exon 7 associated with weak subgroups. Each allele was characterized by a missense or nonsense mutation for which screening by allele-specific primer polymerase chain reaction was performed. The novel mutations were encountered in 28 of the remaining 60 A and B subgroup samples but not among normal donors. As a result of this study, the number of definable alleles associated with weak ABO subgroups has increased from the 14 previously published to 29.

Direct evidence for the existence of Miltenberger antigen.

The Miltenberger (Mi) subsystem, which originally consisted of four phenotypes, now has 11 phenotypes. The antigens of this subsystem belong to the MNS blood group system. The Mia antigen has been reported to be present on red blood cells with several Miltenberger phenotypes, namely: Mi.I, Mi.II, Mi.III, Mi.IV, Mi.VI and Mi.X. However, the existence of the Mia antigen as a separate entity has been in question and difficult to prove with polyclonal reagents. We report the first monoclonal anti-Mia (GAMA210), whose epitope is TNDKHKRD or QTNDMHKR, and thereby confirm the existence of the Mia antigen.

Hypnotizability in acute stress disorder.

OBJECTIVE: This study investigated the relationship between acute dissociative reactions to trauma and hypnotizability. METHOD: Acutely traumatized patients (N=61) with acute stress disorder, subclinical acute stress disorder (no dissociative symptoms), and no acute stress disorder were administered the Stanford Hypnotic Clinical Scale within 4 weeks of their trauma. RESULTS: Although patients with acute stress disorder and patients with subclinical acute stress disorder displayed comparable levels of nondissociative psychopathology, acute stress disorder patients had higher levels of hypnotizability and were more likely to display reversible posthypnotic amnesia than both patients with subclinical acute stress disorder and patients with no acute stress disorder. CONCLUSIONS: The findings may be interpreted in light of a diathesis-stress process mediating trauma-related dissociation. People who develop acute stress disorder in response to traumatic experience may have a stronger ability to experience dissociative phenomena than people who develop subclinical acute stress disorder or no acute stress disorder.

MAM: a "new" high-incidence antigen found on multiple cell lines.

BACKGROUND: Three women have been identified with an antibody to a "new" high-incidence antigen found on multiple cell lines. CASE REPORTS: The proposita, M.A.M., presented during her third pregnancy with an antibody reacting with all RBCs tested except her own. She delivered a thrombocytopenic infant with a 3+ DAT, but without symptoms of HDN. The second example, A.N., presented during her third pregnancy with an antibody reacting with all RBCs tested except her own and those of M.A.M. She delivered a slightly thrombocytopenic but severely anemic infant. The third example, F.K., a sister of A.N., has an antibody reacting with all RBCs tested except her own and those of M.A.M. and A.N. CONCLUSION: This "new" high-incidence antigen has been named MAM and assigned high-incidence antigen number 901016 by the International Society of Blood Transfusion. The corresponding antibody, anti-MAM, has been shown to cause HDN and has the potential to shorten RBC survival after the transfusion of incompatible RBC units, as determined by monocyte monolayer assay. Immunoblotting and flow cytometry show that this new antibody reacts with various WBC lines in addition to RBCs. This antibody also appears to react with platelets in some assays.

A prospective study of psychophysiological arousal, acute stress disorder, and posttraumatic stress disorder.

This study investigated the role of acute arousal in the development of posttraumatic stress disorder (PTSD). Hospitalized motor-vehicle-accident survivors (n = 146) were assessed for acute stress disorder (ASD) within 1 month of the trauma and were reassessed (n = 113) for PTSD 6 months posttrauma. Heart rate (HR) and blood pressure (BP) were assessed on the day of hospital discharge. Participants with subclinical ASD had higher HR than those with ASD and no ASD. Participants who developed PTSD had higher HR in the acute posttrauma phase than those without PTSD. Diagnosis of ASD and resting HR accounted for 36% of the variance of the number of PTSD symptoms. A formula composed of a diagnosis of ASD or a resting HR of > 90 beats per minute possessed strong sensitivity (88%) and specificity (85%) in predicting PTSD. These findings are discussed in terms of acute arousal and longer term adaptation to trauma.