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Incorporation of different antifungal medicaments to commercially available tissue conditioners can be recommended for the management of denture induced stomatitis.

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Background and objectives: Sodium glucose transporter 2 (SGLT2)-inhibitor-induced uric acid lowering may contribute to kidney protective effects of the drug-class in people with type 2 diabetes. This study investigates mechanisms of plasma uric acid lowering by SGLT2-inhibitors in people with type 2 diabetes with a focus on urate transporter (URAT)1. Methods: We conducted an analysis of two randomized, clinical trials. First, in the Renoprotective Effects of Dapagliflozin in Type 2 Diabetes (RED) study, 44 people with type 2 diabetes were randomized to dapagliflozin or gliclazide for 12 weeks. Plasma uric acid, fractional uric acid excretion and hemodynamic kidney function were measured in the fasted state and during clamped eu- or hyperglycemia. Second, in the Uric Acid Excretion study (UREX) study, 10 people with type 2 diabetes received 1-week empagliflozin, benzbromarone and their combination in a cross-over design and effects on plasma uric acid, fractional uric acid excretion and 24-hr uric acid excretion were measured. Results: In the RED study, compared to the fasted state (5.3±1.1mg/dL), acute hyperinsulinemia and hyperglycemia significantly reduced plasma uric acid by 0.2±0.3 and 0.4±0.3 mg/dL (both p<0.001), while increasing fractional uric acid excretion (by 3.2±3.1% and 8.9±4.5% respectively (both p<0.001). Dapagliflozin reduced plasma uric acid by 0.8±0.8mg/dL, 1.0±1.0mg/dL and by 0.8±0.7mg/dL during fasting, hyperinsulinemic-euglycemic and hyperglycemic conditions (p<0.001), whereas fractional uric acid excretion in 24-hr urine increased by 3.0±2.1% (p<0.001) and 2.6±4.5% during hyperinsulinemic-euglycemic conditions (p=0.003). Fractional uric acid excretion strongly correlated to fractional glucose excretion (r= 0.35, p=0.02). In the UREX study, empagliflozin and benzbromarone both significantly reduced plasma uric acid and increased fractional uric acid excretion. Effects of combination therapy did not differ from benzbromarone monotherapy. Conclusion: In conclusion, SGLT2-inhibitors induce uric acid excretion, which is strongly linked to urinary glucose excretion and which is attenuated during concomitant pharmacological blockade of URAT1.

BackgroundNewcastle disease (ND) is one of the most deadly diseases of poultry around the globe. The disease is endemic in Pakistan and recurrent outbreaks are being reported regularly in wild captive, rural and commercial poultry flocks. Though, efforts have been made to characterize the causative agent in some of parts of the country, the genetic nature of strains circulating throughout Pakistan is currently lacking.Material and methodsTo ascertain the genetics of NDV, 452 blood samples were collected from 113 flocks, originating from all the provinces of Pakistan, showing high mortality (30–80%). The samples represented domesticated poultry (broiler, layer and rural) as well as wild captive birds (pigeons, turkeys, pheasants and peacock). Samples were screened with real-time PCR for both matrix and fusion genes (1792 bp), positive samples were subjected to amplification of full fusion gene and subsequent sequencing and phylogenetic analysis.ResultsThe deduced amino acid sequence of the fusion protein cleavage site indicated the presence of motif (112RK/RQRR↓F117) typical for velogenic strains of NDV. Phylogenetic analysis of hypervariable region of the fusion gene indicated that all the isolates belong to lineage 5 of NDV except isolates collected from Khyber Pakhtunkhwa (KPK) province. A higher resolution of the phylogenetic analysis of lineage 5 showed the distribution of Pakistani NDV strains to 5b. However, the isolates from KPK belonged to lineage 4c; the first report of such lineage from this province.ConclusionsTaken together, data indicated the prevalence of multiple lineages of NDV in different poultry population including wild captive birds. Such understanding is crucial to underpin the nature of circulating strains of NDV, their potential for interspecies transmission and disease diagnosis and control strategies.