Effects of Alternate Wet and Dry Conditions on the Mechanical and Physical Performance of Limestone Calcined Clay Cement Mortars Immersed in Sodium Sulfate Media

Sulfate attack in concrete structures significantly reduces their durability. This article reports the experimental findings on the effects of sodium sulfate on limestone calcined clay cement (LC³) in an alternate wet and dry media. The samples underwent wet–dry conditions of 28 cycles. Two types of LC³ were studied, one made from clay (LC³-CL) and the other made from fired rejected clay bricks (LC³-FR). The composition of each LC³ blend by weight was 50% clinker, 30% calcined clay, 15% limestone, and 5% gypsum. The reference compressive strength was evaluated at 2, 7, and 28 days of age. Then, ordinary Portland cement (OPC) and LC³-CL blends were subjected to alternate wet–dry cycle tests, immersion in a 5% sodium sulfate solution, or in water. For all exposed samples, sorptivity tests and compressive strength were done. The results showed that LC³ blends met the requirements for KS-EAS 18-1:2017 standard, which specifies the composition and conformity criteria for common cements in Kenya. The LC³ blend also had a lower rate of initial absorption compared to OPC. Additionally, LC³ blend also showed good resistance to sodium sulfate when exposed to alternating wetting and drying environment. OPC showed higher compressive strength than LC³ blends for testing ages of 2, 7, and 28 days. However, the LC³ samples utilized in the sodium sulfate attack experiment, which were later tested after 84 days, exhibited higher compressive strengths than OPC tested after the same period.     

Type II antithrombin deficiency caused by a large in‐frame insertion: structural,functional and pathological relevance

Summary. Background: The metastable native conformation of serpins is required for their protease inhibition mechanism, but also renders them vulnerable to missense mutations that promote protein misfolding with pathological consequences. Objective: To characterize the first antithrombin deficiency caused by a large in‐frame insertion. Patients/Methods: Functional, biochemical and molecular analysis of the proband and relatives was performed. Recombinant antithrombin was expressed in HEK‐EBNA cells. Plasma and recombinant antithrombins were purified and sequenced by Edman degradation. The stability was evaluated by calorimetry. Reactive centre loop (RCL) exposure was determined by thrombin cleavage. Mutant antithrombin was crystallized as a dimer with latent plasma antithrombin. Results: The patient, with a spontaneous pulmonary embolism, belongs to a family with significant thrombotic history. We identified a complex heterozygous in‐frame insertion of 24 bp in SERPINC1, affecting strand 3 of β‐sheet A, a region highly conserved in serpins. Surprisingly, the insertion resulted in a type II antithrombin deficiency with heparin binding defect. The mutant antithrombin, with a molecular weight of 59 kDa, had a proteolytic cleavage at W49 but maintained the N‐terminal disulphide bonds, and was conformationally sensitive. The variant was non‐inhibitory. Analysis of the crystal structure of the hyperstable recombinant protein showed that the inserted sequence annealed into β‐sheet A as the fourth strand, and maintained a native RCL. Conclusions: This is the first case of a large in frame‐insertion that allows correct folding, glycosylation, and secretion of a serpin, resulting in a conformationally sensitive non‐inhibitory variant, which acquires a hyperstable conformation with a native RCL.     

Acute surgical unit safely reduces unnecessary after-hours cholecystectomy

Introduction

The acute surgical model has been trialled in several institutions with mixed results. The aim of this study was to determine whether the acute surgical model provides better outcomes for patients with acute biliary presentation, compared with the traditional emergency surgery model of care.

Methods

A retrospective review was carried out of patients who were admitted for management of acute biliary presentation, before and after the establishment of an acute surgical unit (ASU). Outcomes measured were time to operation, operating time, after-hours operation (6pm – 8am), length of stay and surgical complications.

Results

A total of 342 patients presented with acute biliary symptoms and were managed operatively. The median time to operation was significantly reduced in the ASU group (32.4 vs 25.4 hours, p=0.047), as were the proportion of operations performed after hours (19.5% vs 2.5%, p<0.001) and the median length of stay (4 vs 3 days, p<0.001). The median operating time, rate of conversion to open cholecystectomy and wound infection rates remained similar.

Conclusions

Implementation of an ASU can lead to objective differences in outcomes for patients who present with acute cholecystitis. In our study, the ASU significantly reduced time to operation, the number of operations performed after hours and length of stay.     

The serological relationships of Nairobi sheep disease virus.

Nairobi sheep disease virus has been shown to be identical with or very closely related to Ganjam virus, which has been isolated from ticks and mosquitoes in India. The virus of NSD also shows some serological relationships on complement-fixation with Dugbe virus and certain strains of Congo.Another Kenyan tick-borne virus shares this close serological relationship with NSD. Some relationships, which are not evident on complement-fixation tests, can be demonstrated by fluorescent antibody or indirect haemagglutination tests between NSD and other strains of Congo and Hazara virus. These would seem to be less significant.     

Role of presynaptic purinoceptors and cyclic AMP on the noradrenaline release in cat cerebral arteries

Field electrical stimulation (ES), K+ (50 mM) or ionophore X-537A (0.01 mM) induced tritium release from cat cerebral arteries preincubated with [3H]noradrenaline (NA). Adenosine and AMP (0.5 mM) did not modify tritium release caused by ionophore X-537A, but these agents and ATP (0.5 mM) significantly reduced that elicited by ES and K+; this reduction was antagonized by 1-methyl-3-isobutylxanthine (MIX; 0.05 mM). Inosine (0.5 mM) and the agonist of purinergic A2-receptors, 5'N-ethyl-carboxamide adenosine (NECA; 0.5 mM) had no effect, but the agonist of purinergic A2-receptors L-N6-phenylisopropyl adenosine (L-PIA; 0.1 mM) diminished tritium efflux caused by ES and K+. The adenosine inhibition of ES-induced radioactivity release was not affected by indomethacin (0.05 mM). MIX (0.05 mM) increased tritium release evoked by ES and K+. Agents that increase intracellular cyclic (c)AMP levels, such as dibutyryl cAMP (0.5 mM), the phosphodiesterase inhibitor Ro 20-1724 (0.1 mM), and the activators of adenylate cyclase, forskolin (0.005 mM) and NaF (2 mM) reduced tritium secretion elicited by ES and K+. However, the intracellular increase of cyclic GMP (cGMP) caused by 8-Br-cGMP did not affect this secretion. Dipyridamole (0.05 mM) and the adenosine deaminase inhibitor erythro-9-2-hydroxy-3 nonyl adenosine (EHNA; 0.1 mM) also produced inhibition of tritium secretion elicited by ES and K+. Dipyridamole reduced both the uptake of [3H]NA and [3H]adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibition of phorbol ester-mediated phenotypic changes in cultured cells by hypoxanthine

Hypoxanthine induces the differentiation of certain transformedcells in vitro, so analyses were undertaken to determine whetherthis purine metabolite might influence the expression of transformedphenotypes induced in normal cells by chemical agents. Chinesehamster embryo cells and human skin fibroblasts in culture weretreated with the promoting agent phorbol-12,13-didecanoate (PDD)with or without prior treatment with 3-methylcholanthrene (MCA),and various phenotypic effects were monitored. Hypoxanthinewas found to inhibit significantly the formation of type IIIfoci and the increase in saturation density observed for Chinesehamster cells treated with MCA plus the phorbol ester. Inosineand the hypoxanthine analogue aUopurinol could also mediatethe effect on saturation density, while xanthosine could not.An increase in the saturation density of human skin fibroblasts,which can be induced by the phorbol ester alone, was also inhibitedby hypoxanthine. There was no significant effect on the growthrate or the intracelhilar nucleotide pools with hypoxanthine-treatedcells. The results suggest that a normal purine metabolite,hypoxanthine, can modulate the expression of transformed phenotypesinduced in vitro by the known tumor promoter PDD. These observationscould help in elucidating the cellular basis for promotion ofcarcinogenesis.