Renal and jejunal absorption of inorganic phosphate (P(i)) increases with dietary P(i) restriction in the rat. The defect in Na(+)-dependent phosphate transporter has been localized to the kidney of the Hyp mice; however, the adaptation to low-P(i) diet in both kidney and jejunum of the Hyp mice has not been well characterized. Therefore, the current studies were designed to characterize the adaptation of renal and jejunal Na(+)-dependent phosphate transport in the Hyp mice and compare it with normal mice. Low-P(i) diet significantly increased the slope of the initial rate of renal brush border membrane (BBM) phosphate uptake compared with corresponding values in mice raised on control-P(i) diet (0.035 vs 0.017) (P < 0.01). Kinetics of renal Na(+)-dependent phosphate uptake in Hyp mice showed a Vmax of 1.00 +/- 0.01 and 0.46 +/- 0.02 nmoles/mg protein/15 sec in low- and control-P(i) diets, respectively (P < 0.01), whereas, Km values were 0.07 +/- 0.04 and 0.02 +/- 0.01, respectively. Similar kinetic analysis in renal BBM of normal mice showed a Vmax of 2.4 +/- 0.17 and 1.18 +/- 0.09 (P < 0.01) and Km of 0.07 +/- 0.03 and 0.08 +/- 0.03 on low and control P(i) diets, respectively. Similarly, low-P(i) diet significantly increased the slope of the initial rate of intestinal phosphate uptake (0.013 and 0.007) (P < 0.01). Kinetics of jejunal Na(+)-dependent phosphate uptake in Hyp mice showed a Vmax of 0.36 +/- 0.01 and 0.2 +/- 0.02 nmoles/mg protein/15 sec, (P < 0.01) and Km of 0.13 +/- 0.06 and 0.06 +/- 0.01 mM in low- and in control-P(i) diet, respectively. Kinetic analysis in jejunal BBM of normal mice showed a Vmax of 0.47 +/- 0.04 and 0.18 +/- 0.01 nmoles/mg protein/15 sec (P < 0.01) and Km of 0.16 +/- 0.04 and 0.11 +/- 0.01 in low- and control-P(i) diets, respectively. The data indicates that low-phosphate diet upregulates the Vmax of the renal and jejunal Na(+)-dependent phosphate cotransporter in the hypophosphatemic mice.
The hypophosphatemic mouse is a useful model for the study of hypophosphatemic vitamin D-resistant rickets in humans. Hypophosphatemia and hyperphosphaturia are the main biochemical findings in the patients and in mice with the disorder. The exact membrane localization of the site of the defect in phosphate transport in humans is not known. We utilized a well-validated technique of brush border and basolateral membrane vesicles to investigate phosphate transport across the enterocyte and the renal tubule cells of the hypophosphatemic (Hyp) mice model. Phosphate uptake by brush border membranes of jejunal enterocytes revealed similar initial rates (slopes were 0.007 and 0.006 for Hyp and control mice, respectively). Kinetics of jejunal Na(+)-dependent phosphate uptake showed a Vmax of 0.21 +/- 0.03 and 0.19 +/- 0.02 nmol/mg protein/15 sec, and Km of 0.12 +/- 0.07 and 0.09 +/- 0.02 mM in the Hyp and control mice, respectively. Kinetics of basolateral uptake of phosphate were also similar (Vmax of 0.05 +/- 0.01 and 0.06 +/- 0.02 nmol/mg protein/10 sec and Km of 0.013 +/- 0.004 and 0.028 +/- 0.022 mM, respectively). On the other hand, kinetics of Na(+)-dependent phosphate uptake by renal brush border membrane vesicles (BBMV) were markedly decreased (Vmax of 0.42 +/- 0.03 and 1.09 +/- 0.06 nmol/mg protein/15 sec, P < 0.01, and Km of 0.01 +/- 0.003 and 0.05 +/- 0.02 mM, P < 0.02, in the Hyp and control mice, respectively). Kinetics of Na(+)-dependent phosphate uptake by renal basolateral membrane were not decreased (Vmax of 0.19 +/- 0.02 and 0.21 +/- 0.02 nmol/mg protein/10 sec and Km of 0.012 +/- 0.003 and 0.012 +/- 0.004 mM for Hyp and control mice, respectively). To determine whether the decrease in renal BBMV is secondary to alteration in the Na(+)-dependent phosphate transporter or due to changes in the Na+ gradient, two studies were conducted: first, a tracer exchange study in renal BBMV which showed a decrease in phosphate uptake in Hyp BBMV compared with controls, confirming the kinetic studies; and second, an Na+ permeability study in renal BBMV of Hyp and control mice which showed no differences in Na+ permeability across the renal BBMV. These findings suggest that the defect in the hypophosphatemic mice is localized only to the brush border membranes of the kidney and is not due to alteration in the driving forces across the membranes.
A 74-year-old man was treated with ceftriaxone for 5 days and subsequently experienced epigastric pain. Computed tomography (CT) was performed 7 and 3 days before epigastralgia. Although the first CT image revealed no radiographic signs in his biliary system, the second CT image revealed dense radiopaque material in the gallbladder lumen. The third CT image, taken at symptom onset, showed high density in the common bile duct and enlargement of the pancreatic head. This is a very rare case of pseudolithiasis involving the common bile duct, as captured on a series of CT images.
A 26-year-old man with right lower mandibular and chest pain, fever, and respiratory distress was urgently transported to our hospital. CT images revealed gas collection and an abscess from the neck to the mediastinum with bilateral pleural effusion. Descending necrotizing mediastinitis (DNM) induced by an odontogenic infection of a right mandibular molar abscess was diagnosed. The cervical and mediastinal areas were drained, extensive debridement was performed, necrotic tissue was excised, and broad-spectrum antibiotics were administered immediately. Prompt diagnosis and intensive care were necessary for managing the DNM, and the patient was discharged with no comorbidities.
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