Aroid scarabs in the genus Peltonotus Burmeister (Coleoptera,Scarabaeidae, Dynastinae): key to species and new distributional data

The southeast Asian scarab beetle genus Peltonotus Burmeister (Scarabaeidae, Dynastinae, Cyclocephalini) is reviewed. New country records for Peltonotus morio Burmeister (Myanmar and Vietnam), Peltonotus nasutus Arrow (southern China and Cambodia), and Peltonotus favonius Jameson and Wada (Myanmar) are reported, including a new record in the Palearctic/Sino-Japanese biogeographic region. The first female specimen of Peltonotus favonius is described. Biological associations with aroid inflorescences are reviewed, and human consumption of Peltonotus beetles is reported. A key to all species, paralectotype designations for Peltonotus nasutus, diagnoses, and distributions using dynamic mapping tools are included.     

Tumor suppressor p53: analysis of wild-type and mutant p53 complexes.

It has been suggested that the dominant effect of mutant p53 on tumor progression may reflect the mutant protein binding to wild-type p53, with inactivation of suppressor function. To date, evidence for wild-type/mutant p53 complexes involves p53 from different species. To investigate wild-type/mutant p53 complexes in relation to natural tumor progression, we sought to identify intraspecific complexes, using murine p53. The mutant phenotype p53-246(0) was used because this phenotype is immunologically distinct from wild-type p53-246+ and thus permits immunological analysis for wild-type/mutant p53 complexes. The p53 proteins were derived from genetically defined p53 cDNAs expressed in vitro and also from phenotypic variants of p53 expressed in vivo. We found that the mutant p53 phenotype was able to form a complex with the wild type when the two p53 variants were cotranslated. When mixed in their native states (after translation), the wild-type and mutant p53 proteins did not exhibit any binding affinity for each other in vitro. Under identical conditions, complexes of wild-type human and murine p53 proteins were formed. For murine p53, both the wild-type and mutant p53 proteins formed high-molecular-weight complexes when translated in vitro. This oligomerization appeared to involve the carboxyl terminus, since truncated p53 (amino acids 1 to 343) did not form complexes. We suggest that the ability of the mutant p53 phenotype to complex with wild type during cotranslation may contribute to the transforming function of activated mutants of p53 in vivo.     

Temperature-dependent switching between "wild-type" and "mutant" forms of p53-Val135

The p53 gene is a suppressor of abnormal cell growth but is also subject to oncogenic activation by mutation. The mutant allele p53-Val135, has recently been discovered to be temperature-sensitive and functions as an oncogene at 37 degrees C and as a tumor suppressor at 32.5 degrees C. In order to investigate the molecular mechanism underlying the temperature sensitivity of p53-Val135 rabbit reticulocyte lysate was used to translate the p53 mRNAs in vitro at 37 degrees C and at 30 degrees C. The immunoreactivity and T antigen binding of wild-type protein p53-Ala135 were unaffected by temperature and were similar to wild-type p53 expressed in vivo. In contrast, the mutant p53-Val135 protein was markedly affected by temperature. At 37 degrees C p53-Val135 showed reduced T antigen binding and did not react with monoclonal antibodies PAb246 and PAb1620. At 30 degrees C, p53-Val135 behaved as the wild-type p53. Temperature also exerted a post-translational effect on p53-Val135 with complete conversion from wild-type to mutant phenotype within two minutes of temperature shift from 30 degrees C to 37 degrees C. There was incomplete conversion from mutant to wild-type phenotype when the temperature was shifted down from 37 degrees C to 30 degrees C. We propose that the temperature dependent forms of p53-Val135 represent conformational variants of the p53 protein with opposing functions in cell growth control.     

Dust and ammonia in horse stalls with different ventilation rates and bedding

Airborne particles and ammonia were monitored in horse stalls managed under four conditions. Two ventilation rates, high (27 air changes per h) and low (5 air changes per h) and two bedding types, paper and straw, were employed. At both ventilation rates, the number of airborne particles generated while the stalls were mucked out was higher with straw than with paper. Particles were more efficiently cleared at the higher ventilation rate in both the straw and paper stalls. Ammonia measurements reflected an accumulation over time. In the stalls with low ventilation, ammonia levels were significantly higher than in those stalls with high ventilation regardless of bedding type. Management decisions and their relationships to respiratory disorders are discussed.     

Mapping and monitoring tick (Acari,Ixodida) distribution,seasonality, and host associations in the United Kingdom between 2017 and 2020

Tick-borne disease risk is intrinsically linked to the distribution of tick vector species. To assess risk and anticipate disease emergence, an understanding of tick distribution, host associations, and seasonality is needed. This can be achieved, to some extent, using passive surveillance supported by engagement with the public, animal health, and public health experts. The Tick Surveillance Scheme (TSS) collects data and maps tick distribution across the United Kingdom (UK). Between 2017 and 2020, 3720 tick records were received and 39 tick species were detected. Most records were acquired in the UK, with a subset associated with recent overseas travel. The dominant UK acquired species was Ixodes ricinus (Ixodida: Ixodidae, Linnaeus), the main vector of Lyme borreliosis. Records peaked during May and June, highlighting a key risk period for tick bites. Other key UK species were detected, including Dermacentor reticulatus (Ixodida: Ixodidae, Fabricius) and Haemaphysalis punctata (Ixodida: Ixodidae, Canestrini & Fanzago) as well as several rarer species that may present novel tick-borne disease risk to humans and other animals. Updated tick distribution maps highlight areas in the UK where tick exposure has occurred. There is evidence of increasing human tick exposure over time, including during the COVID-19 pandemic, but seasonal patterns remain unchanged.     

Fucose-containing polysaccharides in the brown algae Ascophyllum nodosum and Fucus vesiculosus

The fucose-containing, sulfated polysaccharides from Ascophyllum nodosum and Fucus vesiculosus were isolated by extraction with water adjusted to pH 2. Pure fractions were carefully separated by fractional precipitation with ethanol from aqueous solutions containing magnesium or calcium chloride. Progress in the fractionation efforts and purity of the fractions isolated were established by free-boundary and cellulose acetate clectrophoresis. Ascophyllan, two “complexes”, and a galactofucan were isolated from A. nodosum. An ascophyllan-like fraction, and a “complex” were isolated from F. vesiculosus. Mild, acid hydrolysis (0.02m hydrochloric acid, 1 h, 80°) converted each of the “complexes” into an electrophoretically faster-moving and a slower-moving component. The “complex” from F. vesiculosus comprised a greater proportion of the extract than did the two “complexes” from A. nodosum. In addition, the Fucus “complex” was richer in fucose*. However, the data suggest that neither species contains a pure fucan sulfate in the native state.     

Thrombin increases proliferation and decreases fibrinolytic activity of kidney glomerular epithelial cells.

Human glomerular epithelial cells (GECs) in culture synthesize single-chain, urokinase-type plasminogen activator (SC-uPA), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor 1 (PAI-1) and possess specific membrane-binding sites for u-PA. Using purified 125I-alpha thrombin, we demonstrate here the presence of two populations of specific binding sites for thrombin on GECs (1.Kd = 4.3 +/- 1.0 x 10(-10) M, 5.4 +/- 1.4 x 10(4) M sites per cell, 2. Kd = 1.6 +/- 0.5 x 10(-8) M, 7.9 +/- 1.8 x 10(5) sites per cell). Purified human alpha thrombin promoted the proliferation of GECs and induced a time- and dose-dependent increase of SC-uPA, t-PA, and PAI-1 antigens released by GECs. Thrombin-mediated increase in antigen was paralleled by an increase in the levels of corresponding u-PA and PAI-1 messenger RNA. In contrast, thrombin decreased u-PA activity in conditioned medium. This discrepancy between u-PA antigen and u-PA activity was explained by a limited proteolysis of SC-uPA by thrombin, leading to a two-chain form detected by immunoblotting and that could not be activated by plasmin. Thrombin also decreased the number of u-PA binding sites on GECs (p less than 0.05) without changing receptor affinity. Hirudin inhibited the binding and the cellular effects of thrombin, whereas thrombin inactivated by diisopropylfluorophosphate had no effect, indicating that both membrane binding and catalytic activity of thrombin were required. We conclude that thrombin, through specific membrane receptors, stimulates proliferation of GECs and decreases the fibrinolytic activity of GECs both at the cell surface and in the conditioned medium. These results suggest that thrombin could be involved in the pathogenesis of extracapillary proliferation and persistency of fibrin deposits in crescentic glomerulonephritis.