This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To evaluate the effect on blood pressure - measured as changes in systolic and diastolic blood pressure (mmHg) using standardised measurement methods - of substituting sodium salt with other edible salts (e.g. potassium chloride, magnesium chloride) in people with diabetes mellitus.

• MeSH
• Potassium Chloride administration & dosage   MeSH
• Magnesium Chloride administration & dosage   MeSH
• Diabetes Mellitus * MeSH
• Adult MeSH
• Hypertension * diet therapy   MeSH
• Blood Pressure * drug effects   MeSH
• Sodium Chloride, Dietary * administration & dosage   MeSH
• Humans MeSH
• Randomized Controlled Trials as Topic MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Publication type
• Journal Article MeSH

The distribution and morphology of neuronal degeneration were observed and analyzed in each sector of the zona incerta in a lithium‐pilocarpine (LiCl) Wistar rat model of status epilepticus in 12, 15, 18, 21, and 25‐day‐old rats and survival intervals of 4, 8, 12, 24, and 48 hours. Status epilepticus was induced via intraperitoneal (IP) injection of LiCl (3 mmol/kg) 24 hours before an injection of pilocarpine (40 mg/kg, IP). Motor seizures were suppressed by paraldehyde (0.3‐0.6 ml/kg, IP) two hours after status epilepticus onset. Animals were anesthetized using urethane and perfused with phosphate‐buffered saline followed by 4% paraformaldehyde. Brains were sectioned and Nissl stained for map guidance, with fluoro‐Jade B fluorescence used to detect degenerated neurons. Fluoro‐jade B‐positive neurons were plotted to a standard stereotaxic atlas, their distribution was quantified, and their long‐axis diameter was measured. Fluoro‐jade B‐positive neurons were found in pups aged 15 days and older 24 hours after status epilepticus, in which their numbers increased, and their perikaryon size decreased with advancing age. Thus, neuronal damage severity was dependent on age and survival interval. Neuronal damage was only found in the rostral sector of the zona incerta, a region that exhibits a small number of inhibitory neurons and is reciprocally connected to the limbic cortex. This system of hyperactivity, coupled with inhibitory neurons, may be the underlying cause of the neuronal degeneration and explain why it was confined to the rostral sector of the zona incerta.

• MeSH
• Lithium Chloride toxicity   MeSH
• Nerve Degeneration * pathology   etiology   MeSH
• Fluoresceins MeSH
• Rats MeSH
• Disease Models, Animal MeSH
• Neurons * pathology   MeSH
• Animals, Newborn MeSH
• Pilocarpine toxicity   MeSH
• Rats, Wistar MeSH
• Status Epilepticus * pathology   chemically induced   complications   MeSH
• Age Factors MeSH
• Zona Incerta * pathology   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

Biofilm formation is an effective survival strategy of plant-associated microorganisms in hostile environments, so the application of biofilm-forming and exopolysaccharide (EPS)-producing beneficial microbes to plants has received more attention in recent years. This study examined the ability of biofilm and EPS production of Bacillus subtilis and Bacillus thuringiensis strains under different NaCl concentrations (0, 50, 100, 200, and 400 mmol/L), pH values (5.5, 6.5, 7.5, and 8.5), and phosphate levels (0, 25, 50, and 100 mmol/L at 0 and 400 mmol/L NaCl). B. subtilis BS2 and B. thuringiensis BS6/BS7 strains significantly increased biofilm formation in a similar pattern to EPS production under salt stress. B. subtilis BS2/BS3 enhanced biofilm production at slightly acidic pH with a lower EPS production but the other strains formed considerably more amount of biofilm and EPS at alkaline pH. Interestingly, higher levels of phosphate substantially decreased biofilm and EPS production at 0 mmol/L NaCl but increased biofilm formation at 400 mmol/L salt concentration. Overall, contrary to phosphate, salt and pH differently influenced biofilm and EPS production by Bacillus strains. EPS production contributed to biofilm formation to some extent under all the conditions tested. Some Bacillus strains produced more abundant biofilm under salt and pH stress, indicating their potential to form in vivo biofilms in rhizosphere and on plants, particularly under unfavorable conditions.

• MeSH
• Bacillus subtilis physiology   metabolism   drug effects   MeSH
• Bacillus thuringiensis physiology   drug effects   MeSH
• Polysaccharides, Bacterial * metabolism   biosynthesis   MeSH
• Biofilms * drug effects   growth & development   MeSH
• Sodium Chloride * pharmacology   metabolism   MeSH
• Phosphates * metabolism   pharmacology   MeSH
• Hydrogen-Ion Concentration MeSH
• Publication type
• Journal Article MeSH

Cadmium crosses the blood-brain barrier inducing damage to neurons. Cell impairment is predominantly linked to oxidative stress and glutathione (GSH) depletion. On the other hand, several reports have described an increase of GSH levels in neuronal cells after CdCl2 exposure. Therefore, the aim of the present report was to investigate the relation between changes in GSH levels and mitochondrial damage in neuronal cells after CdCl2 treatment. To characterize neuronal impairment after CdCl2 treatment (0-200 μM) for 1-48 h, we used the SH-SY5Y cell line. We analyzed GSH metabolism and determined mitochondrial activity using high-resolution respirometry. CdCl2 treatment induced both the decreases and increases of GSH levels in SH-SY5Y cells. GSH concentration was significantly increased in cells incubated with up to 50 μM CdCl2 but only 100 μM CdCl2 induced GSH depletion linked to increased ROS production. The overexpression of proteins involved in GSH synthesis increased in response to 50 and 100 μM CdCl2 after 6 h. Finally, strong mitochondrial impairment was detected even in 50 μM CdCl2 treated cells after 24 h. We conclude that a significant decrease in mitochondrial activity can be observed in 50 μM CdCl2 even without the occurrence of GSH depletion in SH-SY5Y cells.

• MeSH
• Cadmium Chloride * toxicity   MeSH
• Glutathione * metabolism   MeSH
• Humans MeSH
• Mitochondria * drug effects   metabolism   MeSH
• Cell Line, Tumor MeSH
• Neurons * drug effects   metabolism   MeSH
• Oxidative Stress drug effects   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH

Pilíře léčby cystické fibrózy byly dlouhá léta tvořeny péčí o průchodnost dýchacích cest, agresivní antibiotickou léčbou plicní infekce a vysokokalorickou stravou spolu se suplementací pankreatickými enzymy. V posledních deseti letech je však dostupná modulátorová léčba cílená na jednotlivé patogenní varianty genu pro transmembránový regulátor vodivosti (cystic fibrosis transmembrane conductance regulator, CFTR). Jako vysoce účinnou modulátorovou léčbu pak označujeme terapii ivakaftorem u nosičů tzv. gating mutací (např G551D) a užití kombinace elexakaftor-tezakaftor-ivakaftor u nosičů alespoň jedné mutace F508deL

or many years, the mainstays of cystic fibrosis treatment have been airway patency care, aggressive antibiotic treatment of lung infection, and a high-calorie diet along with pancreatic enzyme supplementation. In the last ten years, however, modulatory treatment targeting individual pathogenic variants of the CFTR gene (cystic fibrosis transmembrane conductance regulator) has become available. As a highly effective modulator treatment, we refer to ivacaftor therapy in carriers of so-called gating mutations (e.g. G551D) and the use of the elexacaftor-tezacaftor-ivacaftor combination in carriers of at least one F508del mutation.

• Keywords
• vysoce účinná modulátorová léčba, ivakaftor, lumakaftor,
• MeSH
• Burkholderia cepacia MeSH
• Chlorides MeSH
• Cystic Fibrosis * drug therapy   genetics   pathology   MeSH
• Drug Therapy, Combination MeSH
• Humans MeSH
• Young Adult MeSH
• Mutation MeSH
• Nutritional Status MeSH
• Sweat chemistry   MeSH
• Cystic Fibrosis Transmembrane Conductance Regulator * genetics   drug effects   MeSH
• Check Tag
• Humans MeSH
• Young Adult MeSH
• Male MeSH
• Publication type
• Case Reports MeSH

BACKGROUND: Glucocorticoids are commonly used in children with different chronic diseases. Growth failure represents a so far untreatable undesired side-effect. As lithium chloride (LiCl) is known to induce cell renewal in various tissues, we hypothesized that LiCl may prevent glucocorticoid-induced growth failure. METHODS: We monitored growth of fetal rat metatarsals cultured ex-vivo with dexamethasone and/or LiCl, while molecular mechanisms were explored through RNA sequencing by implementing the differential gene expression and gene set analysis. Quantification of β-catenin in human growth plate cartilage cultured with dexamethasone and/or LiCl was added for verification. RESULTS: After 14 days of culture, the length of dexamethasone-treated fetal rat metatarsals increased by 1.4 ± 0.2 mm compared to 2.4 ± 0.3 mm in control bones (p < 0.001). The combination of LiCl and dexamethasone led to bone length increase of 1.9 ± 0.3 mm (p < 0.001 vs. dexamethasone alone). By adding lithium, genes for cell cycle and Wnt/β-catenin, Hedgehog and Notch signaling, were upregulated compared to dexamethasone alone group. CONCLUSIONS: LiCl has the potential to partially rescue from dexamethasone-induced bone growth impairment in an ex vivo model. Transcriptomics identified cell renewal and proliferation as candidates for the underlying mechanisms. Our observations may open up the development of a new treatment strategy for bone growth disorders. IMPACT: LiCl is capable to prevent glucocorticoid-induced growth failure in rat metatarsals in vitro. The accompanying drug-induced transcriptomic changes suggested cell renewal and proliferation as candidate underlying mechanisms. Wnt/beta-catenin pathway could be one of those novel mechanisms.

• MeSH
• beta Catenin * metabolism   MeSH
• Lithium Chloride * pharmacology   MeSH
• Dexamethasone * pharmacology   MeSH
• Glucocorticoids pharmacology   MeSH
• Rats MeSH
• Humans MeSH
• Metatarsal Bones * drug effects   MeSH
• Rats, Sprague-Dawley MeSH
• Cell Proliferation drug effects   MeSH
• Growth Plate drug effects   metabolism   MeSH
• Wnt Signaling Pathway drug effects   MeSH
• Bone Development drug effects   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

Exokrinní pankreatická insuficience je podmíněna nedostatečnou sekrecí pankrea­tických enzymů ev. jejich předčasnou inaktivací anebo jejich inadekvátní aktivací ve střevě. Hlavní příčinou u dětí je chronická pankreatitida a cystická fibróza. Klinicky se pankreatická malabsorpce projeví neprospíváním, steatoreou s průjmem, azotoreou s poklesem sérového albuminu a proteinů. Cystická fibróza je nejčastějším autozomálně recesivně dědičným onemocněním kavkazské rasy. Onemocnění má charakter multiorgánového postižení. Prognóza velmi závisí na včasné diagnostice a multioborovém léčebném přístupu. Autoři poukazují na stále platný význam potního testu v diagnostice cystické fibrózy prezentací kazuistiky batolete s cystickou fibrózou s negativním novorozeneckým screeningem.

The cause of exocrine pancreatic insufficiency is inadequate secretion of pancreatic enzymes or premature inactivation or inadequate activation in the bowel. The main cause is chronic pancreatitis and cystitic fibrosis. Clinical manifestations of pancreatic malabsorption are weight loss, steatorrhea with diarrehea, azotorhhea, loss of serum albumin and proteins. Cystic fibrosis is the most common autosomal recessive disease of the Caucasian population characterised by chronic multi-organ impairment. Early diagnosis and multi-professional centre care is necessery for optimal management and improved quality of life and survival of patients. The authors point out the importance of the sweat test in diagnosis of cystic fibrosis presentation of a case study of toddler with cystic fibrosis who had a negative newborn screening.

• MeSH
• Milk Hypersensitivity diagnosis   diet therapy   MeSH
• Amino Acids therapeutic use   MeSH
• Chlorides analysis   MeSH
• Cystic Fibrosis * diagnosis   complications   pathology   therapy   MeSH
• Exocrine Pancreatic Insufficiency * diagnosis   etiology   therapy   MeSH
• Feces enzymology   MeSH
• Infant MeSH
• Humans MeSH
• Neonatal Screening methods   MeSH
• Pancreatic Elastase analysis   MeSH
• Sweat chemistry   MeSH
• Infant Food MeSH
• Check Tag
• Infant MeSH
• Humans MeSH
• Publication type
• Case Reports MeSH

INTRODUCTION: Carp edema virus (CEV) is a fish poxvirus that primarily infects the gills of common carp. CEV causes koi sleepy disease (KSD), which is highly contagious and can result in mortality of up to 100%. METHODS: In the present study, we analyzed the stress and immune responses during KSD in two strains of common carp with different resistance to CEV: susceptible koi and resistant Amur sazan. Experiments were performed at two temperatures: 12°C and 18°C. In the case of koi carp, we also analyzed the effect of supplementation of 0.6% NaCl into tank water, which prevents mortality of the CEV-infected fish (salt rescue model). RESULTS: We found that CEV-infected koi kept at 18°C had the highest viral load, which correlated with the most severe histopathological changes in the gills. CEV infection resulted in the activation of stress response reflected by the upregulated expression of genes involved in stress response in the stress axis organs and increased levels of cortisol and glucose in the blood plasma. These changes were the most pronounced in CEV-infected koi kept at 18°C. At both temperatures, the activation of antiviral immune response was observed in koi kept under freshwater and NaCl conditions upon CEV infection. Interestingly, a clear downregulation of the expression of adaptive immune genes was observed in CEV-infected koi kept under freshwater at 18°C. CONCLUSION: CEV induces a stress response and modulates adaptive immune response in koi, and this is correlated with the level of viral load and disease development.

• MeSH
• Sodium Chloride MeSH
• Edema MeSH
• Immunity MeSH
• Poxviridae Infections * MeSH
• Carps * MeSH
• Fish Diseases * MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Chloride Intracellular Channel (CLIC) family members uniquely transition between soluble and membrane-associated conformations. Despite decades of extensive functional and structural studies, CLICs' function as ion channels remains debated, rendering our understanding of their physiological role incomplete. Here, we expose the function of CLIC5 as a fusogen. We demonstrate that purified CLIC5 directly interacts with the membrane and induces fusion, as reflected by increased liposomal diameter and lipid and content mixing between liposomes. Moreover, we show that this activity is facilitated by acidic pH, a known trigger for CLICs' transition to a membrane-associated conformation, and that increased exposure of the hydrophobic inter-domain interface is crucial for this process. Finally, mutation of a conserved hydrophobic interfacial residue diminishes the fusogenic activity of CLIC5 in vitro and impairs excretory canal extension in C. elegans in vivo. Together, our results unravel the long-sought physiological role of these enigmatic proteins.

• MeSH
• Caenorhabditis elegans * genetics   metabolism   MeSH
• Chloride Channels metabolism   MeSH
• Chlorides * metabolism   MeSH
• Liposomes MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH

• MeSH
• Sodium Chloride * adverse effects   MeSH
• Publication type
• Newspaper Article MeSH
• Interview MeSH