Achieving Stable Nitritation for Mainstream Deammonification by Combining Free Nitrous Acid-Based Sludge Treatment and Oxygen Limitation.

Stable nitritation is a critical bottleneck for achieving autotrophic nitrogen removal using the energy-saving mainstream deammonification process. Herein we report a new strategy to wash out both the Nitrospira sp. and Nitrobacter sp. from the treatment of domestic-strength wastewater. The strategy combines sludge treatment using free nitrous acid (FNA) with dissolved oxygen (DO) control in the nitritation reactor. Initially, the nitrifying reactor achieved full conversion of NH4(+) to NO3(-). Then, nitrite accumulation at ~60% was achieved in the reactor when 1/4 of the sludge was treated daily with FNA at 1.82 mg N/L in a side-stream unit for 24 h. Fluorescence in-situ hybridization (FISH) revealed FNA treatment substantially reduced the abundance of nitrite oxidizing bacteria (NOB) (from 23.0 ± 4.3 to 5.3 ± 1.9%), especially that of Nitrospira sp. (from 15.7 ± 3.9 to 0.4 ± 0.1%). Nitrite accumulation increased to ~80% when the DO concentration in the mainstream reactor was reduced from 2.5-3.0 to 0.3-0.8 mg/L. FISH revealed the DO limitation further reduced the abundance of NOB (to 2.1 ± 1.0%), especially that of Nitrobacter sp. (from 4.9 ± 1.2 to 1.8 ± 0.8%). The strategy developed removes a major barrier for deammonification in low-strength domestic wastewater

Estimated surgical requirements in England after COVID-19: a modelling study using hospital episode statistics

A statistical analysis plan using aggregated, publicly available data from NHS Digital and NHS England to model disruption to, and resources associated with re-establishing, surgical care during the COVID-19 pandemic

Imaging assessment of children presenting with suspected or known juvenile idiopathic arthritis : ESSR-ESPR points to consider

Juvenile idiopathic arthritis (JIA) is the most common paediatric rheumatic disease. It represents a group of heterogenous inflammatory disorders with unknown origin and is a diagnosis of exclusion in which imaging plays an important role. JIA is defined as arthritis of one or more joints that begins before the age of 16 years, persists for more than 6 weeks and is of unknown aetiology and pathophysiology. The clinical goal is early suppression of inflammation to prevent irreversible joint damage which has shifted the emphasis from detecting established joint damage to proactively detecting inflammatory change. This drives the need for imaging techniques that are more sensitive than conventional radiography in the evaluation of inflammatory processes as well as early osteochondral change. Physical examination has limited reliability, even if performed by an experienced clinician, emphasising the importance of imaging to aid in clinical decision-making. On behalf of the European Society of Musculoskeletal Radiology (ESSR) arthritis subcommittee and the European Society of Paediatric Radiology (ESPR) musculoskeletal imaging taskforce, based on literature review and/or expert opinion, we discuss paediatric-specific imaging characteristics of the most commonly involved, in literature best documented and clinically important joints in JIA, namely the temporomandibular joints (TMJs), spine, sacroiliac (SI) joints, wrists, hips and knees, followed by a clinically applicable point to consider for each joint. We will also touch upon controversies in the current literature that remain to be resolved with ongoing research

Platelet CLEC-2 protects against lung injury via effects of its ligand podoplanin on inflammatory alveolar macrophages in the mouse

There is no therapeutic intervention proven to prevent acute respiratory distress syndrome (ARDS). Novel mechanistic insights into the pathophysiology of ARDS are therefore required. Platelets are implicated in regulating many of the pathogenic processes that occur during ARDS; however, the mechanisms remain elusive. The platelet receptor CLEC-2 has been shown to regulate vascular integrity at sites of acute inflammation. Therefore the purpose of this study was to establish the role of CLEC-2 and its ligand podoplanin in a mouse model of ARDS. Platelet-specific CLEC-2-deficient, as well as alveolar epithelial type I cell (AECI)-specific or hematopoietic-specific podoplanin deficient, mice were established using cre-loxP strategies. Combining these with intratracheal (IT) instillations of lipopolysaccharide (LPS), we demonstrate that arterial oxygen saturation decline in response to IT-LPS in platelet-specific CLEC-2-deficient mice is significantly augmented. An increase in bronchoalveolar lavage (BAL) neutrophils and protein was also observed 48 h post-IT-LPS, with significant increases in pro-inflammatory chemokines detected in BAL of platelet-specific CLEC-2-deficient animals. Deletion of podoplanin from hematopoietic cells but not AECIs also reduces lung function and increases pro-inflammatory chemokine expression following IT-LPS. Furthermore, we demonstrate that following IT-LPS, platelets are present in BAL in aggregates with neutrophils, which allows for CLEC-2 interaction with podoplanin expressed on BAL inflammatory alveolar macrophages. Taken together, these data suggest that the platelet CLEC-2-podoplanin signaling axis regulates the severity of lung inflammation in mice and is a possible novel target for therapeutic intervention in patients at risk of developing ARDS. </jats:p

The HOG Pathway Dictates the Short-Term Translational Response after Hyperosmotic Shock

In the global osmoshock translational response in yeast, some gene products were translationally mobilized without transcriptional up-regulation. Conversely, other transcriptionally up-regulated mRNAs were translationally inhibited. Analogous changes occurred on the protein level. These translational responses were strongly dependent on Hog1 and Rck2

Recent advances in ankylosing spondylitis: understanding the disease and management

The term spondyloarthritis refers to a group of immune-mediated diseases characterised by inflammation of the axial skeleton, peripheral joints, and entheses. Ankylosing spondylitis (AS) is the most common and characteristic of these entities and even though it was first described over two centuries ago, the understanding of the underlying disease mechanism remains incomplete. It is known that around 40% of patients with AS have subclinical bowel inflammation, suggesting that the origin of the disease could be in the gut. Also, more genes and new molecules have demonstrated a role in the pathogenesis of AS. In this review, we analyse the latest therapies for spondyloarthritis and the most relevant discoveries over the last three years, together with their implications for different aspects of the disease

Reducing N2O Emission from a Domestic-Strength Nitrifying Culture by Free Nitrous Acid-Based Sludge Treatment.

An increase of nitrite in the domestic-strength range is generally recognized to stimulate nitrous oxide (N2O) production by ammonia-oxidizing bacteria (AOB). It was found in this study, however, that N2O emission from a mainstream nitritation system (cyclic nitrite = 25-45 mg of N/L) that was established by free nitrous acid (FNA)-based sludge treatment was not higher but much lower than that from the initial nitrifying system with full conversion of NH4(+)-N to NO3(-)-N. Under dissolved oxygen (DO) levels of 2.5-3.0 mg/L, N2O emission from the nitritation stage was 76% lower than that from the initial stage. Even when the DO level was reduced to 0.3-0.8 mg/L, N2O emission from the nitritation stage was still 40% lower. An investigation of the mechanism showed that FNA treatment caused a shift of the stimulation threshold of nitrite on N2O emission. At the nitritation stage, the maximal N2O emission factor occurred at ∼16 mg of N/(L of nitrite). However, it increased with increasing nitrite in the range of 0-56 mg of N/L at the initial stage. FNA treatment decreased the biomass-specific N2O production rate, suggesting that the enzymes relevant to nitrifier denitrification were inhibited. Microbial analysis revealed that FNA treatment decreased the microbial community diversity but increased the abundances of AOB and denitrifiers

Pharmacognostical and phytochemical evaluation of <i style="mso-bidi-font-style:normal">Cinnamomum wightii </i>Meissn. flowers

33-39<i style="mso-bidi-font-style: normal">Cinnamomum wightii Meissn. (Family <span style="font-family:Symbol;mso-ascii-font-family: " times="" new="" roman";mso-hansi-font-family:"times="" roman";mso-char-type:symbol;="" mso-symbol-font-family:symbol"="" lang="EN-GB">¾ Lauraceae) is a tree mainly found in the Western Ghats and Shola forest of the South India. Pharmacognostical and phytochemical evaluation of crude drug has been done as per WHO guidelines and IHP 2002. The crude flower buds are globoid to round in shape, dark brown with 1-2 cm long pedicel. Transverse section through petals showed both the outer and inner epidermis with numerous stone cells and secretory glands scattered in the cortex. The quantitative values found are: foreign organic matter (0.71%), loss on drying (11.88%), total ash (6.41%), acid insoluble ash (2.07%), water soluble ash (0.38%), alcohol soluble extractive (28.63%) and water soluble extractive (7.23%), foaming index (200), swelling index (0.85 ml), volatile oil content (0.20%) and pesticide residue content. The powdered crude flower buds have shown the presence of stone cells, vessel element, covering trichomes, spiral xylem vessel and fragments of anthers filamentous cell layer. Phytochemical screening of methanolic extract showed the presence of alkaloids, glycosides, flavonoids, saponins, coumarins, reducing sugars, phenolics, tannins, sterols and mucilage. Quantitative estimation of the methanolic extracts of various phytoconstituents, viz. total tannins (156.5 mg/g), total phenolics (146.40 mg/g), total flavonoids (30 mg/g) and total flavonols (3.6 mg/g) content has been estimated spectrophotometrically. These findings may serve as diagnostic tools for identification of the crude drug. </span