UNASSIGNED: Neuromyelitis optica spectrum disorder (NMOSD) is a relatively new terminology composed to encompass patients with neuromyelitis optica (NMO) and related immunological conditions. The diagnosis of this condition requires a seropositive aquaporin-4 immunoglobulin G (AQP-4 IgG), the presence of at least one core clinical characteristic and the exclusion of alternative diagnoses. Very few cases have been reported in sub-Saharan Africa.
UNASSIGNED: The aim of this article is to report a classical case of NMOSD with AQP-4 IgG seropositivity and normal brain, cervical and thoracic MRI findings.
UNASSIGNED: We report a 25-year-old Nigerian woman who presented with recurrent and alternating weakness, pain and numbness of all limbs, associated with episodic painful left-sided tonic spasms and urinary incontinence. She had earlier had symptoms of recurrent, episodic and alternating loss of vision in both eyes, associated with ocular pain.Examination findings revealed an intact mental status, no cranial nerve deficit and no focal limb weakness. Right-sided deep tendon reflexes were exaggerated. Vital signs were within normal limits. Brain MRI, Cervical spine MRI and Thoracic spine MRI all revealed normal findings. Serum aquaporin-4 IgG assay returned positive with a titer of 1:32.She was commenced on high dose steroids and there was gradual improvement of symptoms.
UNASSIGNED: These findings confirmed the diagnosis of neuromyelitis optica spectrum disorder, and satisfies the diagnostic criteria published in 2015 by the International Panel for NMO Diagnosis (IPND).

CONCLUSIONS: Plant Biomarkers are objective indicators of a plant\'s cellular state in response to abiotic and biotic stress factors. They can be explored in crop breeding and engineering to produce stress-tolerant crop species. Global food production safely and sustainably remains a top priority to feed the ever-growing human population, expected to reach 10 billion by 2050. However, abiotic and biotic stress factors negatively impact food production systems, causing between 70 and 100% reduction in crop yield. Understanding the plant stress responses is critical for developing novel crops that can adapt better to various adverse environmental conditions. Using plant biomarkers as measurable indicators of a plant\'s cellular response to external stimuli could serve as early warning signals to detect stresses before severe damage occurs. Plant biomarkers have received considerable attention in the last decade as pre-stress indicators for various economically important food crops. This review discusses some biomarkers associated with abiotic and biotic stress conditions and highlights their importance in developing stress-resilient crops. In addition, we highlighted some factors influencing the expression of biomarkers in crop plants under stress. The information presented in this review would educate plant researchers, breeders, and agronomists on the significance of plant biomarkers in stress biology research, which is essential for improving plant growth and yield toward sustainable food production.

Treating malignant glioma is challenging owing to its highly invasive potential in healthy brain tissue and the formation of intense surrounding edema. Peritumoral edema in gliomas can lead to severe symptoms including neurological dysfunction and brain herniation. For the past 50 years, the standard treatment for peritumoral edema has been steroid therapy. However, the discovery of cerebral lymphatic vessels a decade ago prompted a re-evaluation of the mechanisms involved in brain fluid regulation and the formation of cerebral edema. This review aimed to describe the clinical features of peritumoral edema in gliomas. The mechanisms currently known to cause glioma-related edema are summarized, the limitations in current cerebral edema therapies are discussed, and the prospects for future cerebral edema therapies are presented. Further research concerning edema surrounding gliomas is needed to enhance patient prognosis and improve treatment efficacy.

BACKGROUND: Primary Sjögren\'s syndrome (SS) is a chronic systemic autoimmune disease with varied neurological manifestations. SS is associated with anti-aquaporin-4 antibody (AQP4-IgG)-positive neuromyelitis optica spectrum disorder (NMOSD), a demyelinating autoimmune disorder of the central nervous system (CNS). Intriguingly, there are reports of osmotic demyelinating syndrome (ODS), a supposedly non-inflammatory disorder, in the context of SS and renal tubular acidosis (RTA), both of which are not yet established risk factors for ODS.
METHODS: A literature search was undertaken to identify case reports of ODS in patients with SS. Details of the clinical and laboratory features of these patients were compiled. Additionally, we searched for NMOSD in patients with SS. We looked for co-existing RTA in patients with SS-ODS as well as SS-NMOSD. We also screened for reports of ODS in RTA without underlying SS.
CONCLUSIONS: We identified 15 patients (all women, median age 40 years) with ODS in SS, and all of these patients had comorbid RTA. There were only three reported cases of ODS in RTA without underlying SS. We identified a total of 67 patients with SS-NMOSD, of whom only 3 (4.5%) had RTA. Hence, unlike NMOSD, the development of ODS in SS requires a prolonged osmotic or electrolyte abnormality caused by the comorbid RTA. The 15 patients with ODS and SS -RTA, showed heterogeneous clinical manifestations and outcomes. The most common symptom was quadriparesis, seen in 14 of the 15 patients. Eleven of the 15 patients had one of the following features, either alone or in combination: worsening of the sensorium, extensor plantar response, dysphagia/dysarthria, and facial palsy. The latter four manifestations were present at the onset in 7 patients and later in the course of the illness in the remaining 4 patients. Ocular palsy was seen in only four of the 15 patients and was a late manifestation. One patient who had extensive long-segment myelitis and subsequent ODS died, but most patients recovered without significant sequelae. None had hyponatremia, while all patients had hypokalemia and/or hypernatremia. Hypokalemia causing nephrogenic diabetes insipidus (NDI) followed by rapid rise in sodium and the resultant osmotic stress could potentially explain the occurrence of ODS in SS-RTA. Aquaporin (AQP) in astrocytes is implicated in ODS, and renal AQP is downregulated in NDI. Antibodies against AQPs are present in some patients with SS. Defective AQP is therefore a common link underlying all the connected diseases, namely SS, NDI, and ODS, raising the possibility of immune-mediated AQP dysfunction in the pathogenesis.
CONCLUSIONS: The hitherto unreported association between SS-RTA and ODS may implicate SS and/or RTA in the development of ODS. In the setting of SS-RTA, ODS must be suspected when a patient with flaccid quadriparesis does not respond to the correction of potassium or develops additional neurological features along with a rise in sodium. Defective functions of AQPs may be a possible mechanism linking demyelinating CNS lesions, SS, and RTA. Studies evaluating AQP functions and serum antibodies against AQPs in these conditions are warranted.

The symbiotic relationship between the host and the rumen microbiome plays a crucial role in ruminant physiology. One of the most important processes enabling this relationship is urea nitrogen salvaging (UNS). This process is important for both maintaining ruminant nitrogen balance and supporting production of their major energy supply, bacterially-derived short chain fatty acids (SCFA). The key step in UNS is the trans-epithelial movement of urea across the ruminal wall and this is a highly regulated process. At the molecular level, the key transport route is via the facilitative urea transporter-B2, localized to ruminal papillae epithelial layers. Additional urea transport through aquaporins (AQP), such as AQP3, is now also viewed as important. Long-term regulation of these ruminal urea transport proteins appears to mainly involve dietary fermentable carbohydrates; whereas, transepithelial urea transport is finely regulated by local conditions, such as CO2 levels, pH and SCFA concentration. Although the key principles of ruminal urea transport physiology are now understood, there remains much that is unknown regarding the regulatory pathways. One reason for this is the limited number of techniques currently used in many studies in the field. Therefore, future research in this area that combines a greater range of techniques could facilitate improvements to livestock efficiency, and potentially, reductions in the levels of waste nitrogen entering the environment.

Sjögren\'s syndrome (SS) is an autoimmune disorder that affects the salivary glands, leading to reduced secretory functions and oral and ocular dryness. The salivary glands are composed of acinar cells that are responsible for the secretion and production of secretory granules, which contain salivary components, such as amylase, mucins and immunoglobulins. This secretion process involves secretory vesicle trafficking, docking, priming and membrane fusion. A failure during any of the steps in exocytosis in the salivary glands results in the altered secretion of saliva. Soluble N-ethylmaleimide-sensitive-factor attachment protein receptors, actin, tight junctions and aquaporin 5 all serve an important role in the trafficking regulation of secretory vesicles in the secretion of saliva via exocytosis. Alterations in the expression and distribution of these selected proteins leads to salivary gland dysfunction, including SS. Several studies have demonstrated that green tea polyphenols, most notably Epigallocatechin gallate (EGCG), possess both anti-inflammatory and anti-apoptotic properties in normal human cells. Molecular, cellular and animal studies have indicated that EGCG can provide protective effects against autoimmune and inflammatory reactions in salivary glands in diseases such as SS. The aim of the present article is to provide a comprehensive and up-to-date review on the possible therapeutic interactions between EGCG and the selected molecular mechanisms associated with SS.

BACKGROUND: Glymphatic fluid circulation may be considered the lymphatic system of the brain and the main role of such system seems to be played by aquaporins (AQPs), a family of proteins which regulates water exchange, in particular AQP4 and 1. Alterations of glymphatic fluid circulation through AQPs variations are now emerging as central elements in the pathophysiology of different brain conditions, like hydrocephalus. This systematic review provides an insight about the role of AQPs in hydrocephalus establishment and compensation, investigating their possible role as diagnostic tools or therapeutic targets.
METHODS: PubMed database was screened searching for the relevant existing literature in English language published until February 29th 2020, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Statement.
RESULTS: A total of 40 articles met the inclusion criteria for our systematic analysis. AQP4 resulted the most studied water channel, followed by AQP1. The changes in cerebrospinal fluid (CSF), brain parenchyma and choroid plexus (CP) in different hydrocephalus type were analyzed. Moreover, important pharmacological interactions regarding AQP and molecules or conditions were discussed. A very interesting result is the general consensus on increase of AQP4 in hydrocephalic patients, unless in patients suffering from idiopathic normal pressure hydrocephalus, where AQP4 shows a tendency in reduction.
CONCLUSIONS: AQP seem to play a central role in the pathophysiology of hydrocephalus and in its compensation mechanisms. Further studies are required to definitively establish their precise roles and their quantitative changes to allow their utilization as diagnostic tools or therapeutic targets.

Plant aquaporins (AQPs) of the plasma membrane intrinsic protein (PIP) family face constant risk of hijack by pathogens aiming to infect plants. PIPs can also be involved in plant immunity against infection. This review will utilize two case studies to discuss biochemical and structural mechanisms that govern the functions of PIPs in the regulation of plant infection and immunity. The first example concerns the interaction between rice Oryza sativa and the bacterial blight pathogen Xanthomonas oryzae pv. oryzae (Xoo). To infect rice, Xoo uses the type III (T3) secretion system to secrete the proteic translocator Hpa1, and Hpa1 subsequently mediates the translocation of T3 effectors secreted by this system. Once shifted from bacteria into rice cells, effectors exert virulent or avirulent effects depending on the susceptibility of the rice varieties. The translocator function of Hpa1 requires cooperation with OsPIP1;3, the rice interactor of Hpa1. This role of OsPIP1;3 is related to regulatory models of effector translocation. The regulatory models have been proposed as, translocon-dependent delivery, translocon-independent pore formation, and effector endocytosis with membrane protein/lipid trafficking. The second case study includes the interaction of Hpa1 with the H2O2 transport channel AtPIP1;4, and the associated consequence for H2O2 signal transduction of immunity pathways in Arabidopsis thaliana, a non-host of Xoo. H2O2 is generated in the apoplast upon induction by a pathogen or microbial pattern. H2O2 from this source translocates quickly into Arabidopsis cells, where it interacts with pathways of intracellular immunity to confer plant resistance against diseases. To expedite H2O2 transport, AtPIP1;4 must adopt a specific conformation in a number of ways, including channel width extension through amino acid interactions and selectivity for H2O2 through amino acid protonation and tautomeric reactions. Both topics will reference relevant studies, conducted on other organisms and AQPs, to highlight possible mechanisms of T3 effector translocation currently under debate, and highlight the structural basis of AtPIP1;4 in H2O2 transport facilitated by gating and trafficking regulation.

Otitis media (OM) refers to inflammatory diseases of the middle ear (ME), regardless of cause or pathological mechanism. Among the molecular biological studies assessing the pathology of OM are investigations of the expression of aquaporins (AQPs) in the ME and Eustachian tube (ET). To date, fifteen studies have evaluated AQPs expression in the ME and ET. Although the expression of individual AQPs varies by species and model, eleven types of AQP, AQP1 to AQP11, were found to be expressed in mammalian ME and ET. The review showed that: (1) various types of AQPs are expressed in the ME and ET; (2) AQP expression may vary by species; and (3) the distribution and levels of expression of AQPs may depend on the presence or absence of inflammation, with variations even in the same species and same tissue. Fluid accumulation in the ME and ET is a common pathological mechanism for all types of OM, causing edema in the tissue and inducing inflammation, thereby possibly involving various AQPs. The expression patterns of several AQPs, especially AQP1, 4 and 5, were found to be altered in response to inflammatory stimuli, including lipopolysaccharide (LPS), suggesting that AQPs may have immunological functions in OM.

The evolution of neuromyelitis optica spectrum disorder (NMOSD) from a rare, incurable and misunderstood disease with almost universally poor outcomes to its present state in just over a decade is unprecedented in neurology and possibly in medicine. Our knowledge of NMOSD biology has led to the recognition of wider phenotypes, new disease mechanisms, and thus clinical trials of new and effective treatments. This article aims to update readers on the recent developments in NMOSD with particular emphasis on clinical advances, the 2015 diagnostic criteria, biomarkers, imaging, and therapeutic interventions.