Involvement of F-actin in chaperonin-containing t-complex 1 beta regulating mouse mesangial cell functions in a glucose-induction cell model.

The aim of this study is to investigate the role of chaperonin-containing t-complex polypeptide 1 beta (CCT2) in the regulation of mouse mesangial cell (mMC) contraction, proliferation, and migration with filamentous/globular-(F/G-) actin ratio under high glucose induction. A low CCT2 mMC model induced by treatment of small interference RNA was established. Groups with and without low CCT2 induction examined in normal and high (H) glucose conditions revealed the following major results: (1) low CCT2 or H glucose showed the ability to attenuate F/G-actin ratio; (2) groups with low F/G-actin ratio all showed less cell contraction; (3) suppression of CCT2 may reduce the proliferation and migration which were originally induced by H glucose. In conclusion, CCT2 can be used as a specific regulator for mMC contraction, proliferation, and migration affected by glucose, which mechanism may involve the alteration of F-actin, particularly for cell contraction.

Potassium chloride supplementation alone may not improve hypokalemia in thyrotoxic hypokalemic periodic paralysis.

This article reports a 29-year-old man who came to the Emergency Department because of sudden onset of bilateral lower extremity weakness and inability to walk after intake of a high carbohydrate meal and alcohol. He was found to have severe hypokalemia, with K(+) level at 1.7 mmol/L. However, after administration of potassium chloride (KCl), 10 mEq/h intravenous (i.v.) drip for 4 h, follow-up serum potassium was even lower at 1.5 mmol/L and the patient complained of persistent weakness. Twenty mg of propranolol, a non-selective beta-blocker, was given orally and a dramatic improvement of muscle power to grade 5 was noted after 30 min of administration. On the fifth day after discharge, he had another episode of bilateral lower extremity weakness after ingesting a mouthful of alcohol. Muscle power recovered completely after i.v. drip of KCl, 20 mEq. Laboratory data revealed an underlying primary hyperthyroidism for which he was given anti-thyroid agents and beta-blockers.

Effects of calcitriol on type 5b tartrate-resistant acid phosphatase and interleukin-6 in secondary hyperparathyroidism.

BACKGROUND/AIMS: Secondary hyperparathyroidism (SHP) is characterized by high bone turnover and elevated serum bone remodeling markers. Elevation of serum interleukin-6 (IL-6) levels is also characteristic of end-stage renal disease. This study investigates the effects of intravenous calcitriol on serum bone resorptive markers, namely, type 5b tartrate-resistant acid phosphatase (TRACP5b) and IL-6 in patients with SHP. METHODS: Intravenous calcitriol therapy was given for 16 weeks to 24 patients on maintenance hemodialysis with plasma intact parathyroid hormone (iPTH) levels >300 pg/ml. Blood was drawn at baseline and every 4 weeks for 16 weeks for determination of the levels of biochemical parameters, iPTH, IL-6 and bone remodeling markers, including bone-specific alkaline phosphatase (bAP) and TRACP5b. RESULTS: Only 21 patients responded to the calcitriol therapy, with significant decrements in serum iPTH after 4 weeks of therapy and thereafter. After 16 weeks of calcitriol therapy, 21 patients had significant decrements in serum iPTH (707.9 +/- 317.8 vs. 205.0 +/- 63.1 pg/ml, p < 0.01). Prior to treatment, a significant correlation was found between increased levels of serum iPTH and IL-6 levels (r = 0.45, p < 0.05). After treatment, there was also a significant and parallel lowering of levels of serum iPTH, IL-6 (8.52 +/- 3.59 vs. 7.24 +/- 2.81 pg/ml, p < 0.01), bAP (54.68 +/- 36.17 vs. 24.55 +/- 13.84 U/l, p < 0.01) and TRACP5b (3.41 +/- 1.89 vs. 1.80 +/- 0.55 U/l, p < 0.01). Our results additionally showed significant positive correlationsbetween baseline levels of serum IL-6 and those of iPTH, bAP and TRACP5b. After 16 weeks of calcitriol treatment, the correlation between IL-6 and iPTH levels lost significance but levels of serum IL-6, bAP and TRACP5b remained significantly correlated. CONCLUSIONS: Elevated levels of serum IL-6 and bone remodeling markers, namely, bAP and TRACP5b which are common features of SHP, are effectively suppressed by calcitriol therapy. This indicates that hyperparathyroidism not only accelerates bone remodeling but may also aggravate inflammation in patients on maintenance hemodialysis.

Enhanced expression of glucose transporter 1 on erythrocyte membrane in hemodialysis patients: the possible role in erythrocyte ascorbate recycling.

BACKGROUND: Human erythrocytes can take up dehydroascorbate on the glucose transporter 1 (GLUT 1) and reduce it to ascorbate. Intraerythrocyte ascorbate was proved to be directly responsible for decreased oxidation of extraerythrocytic ascorbate. In addition to spontaneous and irreversible loss of ascorbate in plasma, the hemodialysis (HD) process itself consumes plasma ascorbate. However, intraerythrocyte ascorbate status in uremic patients during HD has yet to be reported. METHODS: Plasma and intraerythrocyte ascorbate, dehydroascorbate, GLUT 1 expression on erythrocyte membranes, and in vitro studies of "erythrocyte ascorbate recycling" were investigated in age- and sex-matched healthy subjects (control group) and HD patients (HD group). RESULTS: Intraerythrocyte ascorbate concentrations decreased after 1 HD session compared with pre-HD and recovered to pre-HD values 2 days later, whereas plasma ascorbate concentrations did not recover. In vitro studies suggested that erythrocytes of HD patients have a stronger ability to maintain intracellular ascorbate concentrations compared with healthy subjects. This ability could be inhibited by cytochalasin B (GLUT 1 inhibitor). We also found increased GLUT 1 expression (P = 0.002) on erythrocyte membranes in the HD group compared with the control group. CONCLUSION: Erythrocytes of uremic patients lost large amounts of ascorbate during HD, but regained it to the pre-HD level 2 days later. Enhanced GLUT 1 expression on erythrocyte membranes for HD patients may contribute to better preservation of intracellular ascorbate compared with healthy subjects.

Axillary supernumerary breast in a female adolescent: report of one case.

Polythelia and polymastia usually occur along the embryonic milk lines extending from the axilla to the groin. Polymastia in female patients has been reported to manifest during pregnancy or lactation. We report a 14-year-old adolescent with axillary supernumerary breasts. She had painful axillary swelling during menstrual period. The mass in the right axilla was excised with pathologic report of supernumerary breasts with fibrocystic change. When a mass is located along the milk line, the possibility of the presence of breast tissue should be considered.

Acute effect of pamidronate on PTH secretion in postmenopausal hemodialysis patients with secondary hyperparathyroidism.

BACKGROUND: The purpose of this study is to evaluate the acute effect of pamidronate on plasma ionized calcium (iCa) level reduction and dynamic parathyroid hormone (PTH) secretion in postmenopausal hemodialysis-dependent women with secondary hyperparathyroidism. METHODS: Twelve postmenopausal women undergoing regular hemodialysis with serum intact PTH levels greater than 200 pg/mL (200 ng/L) were included in this study. Pamidronate was administered intravenously as a single dose of 15 mg in the last hour of hemodialysis. PTH responses to hypocalcemia and hypercalcemia induced with 1 mEq/L (0.5 mmol/L) and 4 mEq/L (2 mmol/L) of dialysate calcium, respectively, were evaluated before and 1 week after pamidronate therapy. RESULTS: Pamidronate therapy resulted in a decrease in predialysis basal plasma iCa (iCa(base); P < 0.05) levels and an increase in maximal serum PTH (PTHmax; P < 0.001), basal PTH (PTHbase; P < 0.001), and minimal PTH levels (P < 0.001). The set point of serum calcium and the slope of the PTH-calcium curve were not altered by pamidronate therapy. An inverse correlation was present between iCa(base) and the PTHbase-PTHmax ratio before (r = -0.66; P < 0.05) and after (r = -0.84; P < 0.001) pamidronate therapy. CONCLUSION: Our study shows that pamidronate therapy is associated with reduced plasma iCa levels and increased PTH secretion, resulting in aggravated secondary hyperparathyroidism. These findings suggest that secondary hyperparathyroidism may worsen after the administration of pamidronate, at least in the short term, in postmenopausal hemodialysis patients.