Decreased anion gap associated with monoclonal and pseudomonoclonal gammopathy.

Nine patients with monoclonal and one with pseudomonoclonal gammopathy were found to have a decreased anion gap. Eight of the patients had multiple myeloma, one has plasma cell leukemia and one had chronic active hepatitis. In all of the the decreased anion gap was associated with an increased concentration of IgG greater than 5 g/dl.     

Imbalances of T-cell subsets in monoclonal gammopathies

Summary In 42 patients with untreated or treated multiple myeloma (MM) or benign monoclonal gammopathy (BMG) the lymphocytes and T lymphocyte subsets were determined by monoclonal antibodies and other surface markers.In untreated MM, the T cells (1077/l vs 1439/l, P<0.01) and especially the OKT4⁺ lymphocytes (700/l vs 950/l, P<0.05) were significantly reduced compared with a control group. The OKT8⁺ cells were slightly but not significantly decreased.In previously treated MM, the loss of T cells was more pronounced than in the untreated group and was primarily caused by a further reduction of OKT4⁺ cells. Patients with BMG revealed decreased OKT8⁺ lymphocytes (304/l vs 502/l, P<0.001), whereas the OKT4⁺ cells were within the normal range. Therefore, the OKT4/OKT8 ratio was significantly elevated compared with that in untreated MM patients and normal controls (3.31 vs 2.06 vs 2.13; P<0.005).To sum up, in MM the results revealed a reduction of T cells, mainly of OKT4⁺ cells, which is intensified by chemotherapy and persists even after a long therapy-free interval. The different findings of T cell subsets in BMG and MM may be a helpful criterion to differentiate between BMG and MM.     

Incidence of monoclonal gammopathies in blood donors]

A routine screening of monoclonal gammopathies (M.G.) was performed in the serum from 36, 015 blood donors by cellulose acetate electrophoresis. The incidence of M.G. was estimated to 0.14 per cent. About 86 per cent of cases can be classified as asymptomatic M.G. and 14 per cent as malignant M.G. (myeloma or Waldenstr?m macroglobulinemia). In asymptomatic forms, heavy chain classes are only IgG or IgM with a large predominance of IgG (86,4%). It is suggested that donors in whom M.G. have been detected should not be allowed to give blood. A yearly clinical, hematological and an immunoglobulin check-up is recommended to these patients in order to defect the first sign of a malignant process.     

Variability of plasma viscosity in monoclonal IgM gammopathies.

Hyperviscosity syndromes can caused by both plasmatic and cellular factors. We have studied 20 patients affected by IgM gammopathy of different origin and 12 healthy subjects matched for sex and age, in order to evaluate the relation between paraprotein levels and plasma viscosity. We have observed a significant plasma viscosity increase only in 14 patients with monoclonal IgMk gammopathy. In the same patients was also evident an hyperviscosity syndrome. In the other 6 patients, with monoclonal IgM or polyclonal gammopathy and without clinical symptoms, plasma viscosity was only slightly increased. We have also observed a significant correlation between IgM and light chains (kappa, lambda) serum level and increased plasma viscosity. These results suggest that one can't consider all IgM gammopathies as cause of hyperviscosity syndrome.     

Serum beta 2-microglobulin in patients with monoclonal gammopathies

Beta-2-microglobulin concentrations were determined in serum samples from 45 patients with benign and malignant monoclonal gammopathies. In the group of patients suffering from multiple myeloma or Waldenstr?m macroglobulinemia the mean beta 2-microglobulin level was significantly higher than in the group with monoclonal gammopathy of undetermined significance. Values above 3 mg/L were highly indicative of a neoplastic process and were observed in all the Waldenstr?m patients and in greater than 90% of myeloma patients. No significant correlation was noticed between beta 2-microglobulin and monoclonal protein levels in any of the groups examined.     

叠氮钠损伤的神经元内硫氧还蛋白mRNA水平的变化

氧化应激与许多神经退变病有关,而线粒体损伤是氧化应激加剧的重要原因。本文通过细胞活性检测（MTT法）、形态学观察,分析NaN3对原代培养神经元的损伤作用,并通过RT－PCR半定量检测NaN3损伤后神经元内硫氧还蛋白（Thioredoxin,Trx)mRNA水平的改变,以阐明这一重要的氧还调节蛋白在神经元损伤过程中的作用。实验表明NaN3以浓度和时间依赖方式损伤神经元,降低Trx表达水平。提示：神经元内呼吸链受损引起Trx表达减少,从而减弱神经元内氧还调节功能,最终引起神经元损伤、死亡。     

Changes in serum copper level during detoxification of acutely poisoned drug addicts

Although it is known that drug addicts are a high-risk group for disruption of many homeostatic processes, little is know about changes in serum trace elements concentrations after taking the psychoactive substances. The aim of the study was to check the influence of the taking homemade heroin on serum level of copper. Blood samples were taken from 30 opiate addicts, and copper concentrations were measured by the means of atomic absorption spectrophotometry. The result of the study show that in the examined group, copper serum concentrations (1.35 mg/L) upon admission to the clinic were higher than in the control group (1.11 mg/L) but decreased during hospitalization (1.18 mg/L). There was no correlation between duration of stay at the hospital and changes in serum copper concentration.     

Role of anion gap and different electrolytes in hypertension during pregnancy (preeclampsia)

The present study was designed to determine the changes in serum sodium, anion gap, different antioxidants and free radicals in preeclamptic patients and control subjects. Serum sodium, chloride, bicarbonate, calcium, potassium and magnesium were estimated and anion gap was determined in 100 proteinuric hypertensive and 100 normotensive pregnant women. Mean serum sodium, chloride and bicarbonate level (133.26 ± 13.1, 104.97 ± 11.37, and 22.01 ± 4.66 mEq/l, respectively) were significantly higher in proteinuric hypertensive women as compared to controls (125.85 ± 10.4, 101.90 ± 6.3, 19.34 ± 3.21 mEq/l, respectively) whereas anion gap level (6.28 ± 16.147) was nonsignificantly higher in proteinuric hypertensive as compared to normotensive (4.61 ± 11.84). Total serum sodium concentration increases in preeclamptic subjects, the exact distribution of serum sodium in various compartments of the body are not clear and correlation of serum sodium and anion gap with proteinuria is also not known. The levels of different antioxidants were decreased in preeclamptic patients as compared to the controls while the level of free radicals elevated in preeclamptic subjects as compared to controls. In our study, anion gap level was found to be rather non-significantly higher in proteinuric hypertensive women as compared to normotensive women.     

Changes in sodium pump transport activity and Na+, K+-ATPase expression level following lymphocytes activation in humans

Ouabain-inhibitable rubidium influxes, intracellular sodium content (Nai), and alpha 1-subunit abundance have been studied in human blood lymphocytes, stimulated by phytohemagglutinin (PHA) or by the phorbol 12,13-dibutyrate (PDBu), and calcium ionophore--ionomycin. It is shown that at early stages of PHA-induced activation, the Na/K pump expression (as determined by Wesrn blots of alpha 1 protein in membrane fractions of total cell lysates) does not change, and the increase in Rb influx is due to the increase in Nai and results from the enhanced transport activity of Na/K pumps present in plasma membrane. During the late stages of G0-->G1-->S transit (16-48 h), the increase in Rb influx occurs without changes in Nai, and monensin increases both Nai, and the Rb influx via the Na/K pump. To the end of the first day of mitogen activation, the alpha 1 protein content was found to increase by 5-7 times. A correlation was revealed between changes in ouabain-inhibitable Rb influxes, alpha 1 protein abundance, and the proliferation rate. It is concluded that blasttransformathion of normal human lymphocytes is accompanied by the increase in membrane-associated pool of alpha 1-subunit of Na+,K(+)-ATPase, and the enhanced activity of sodium pump during the G0-->G1-->S progression is provided by increased number of Na+,K(+)-ATPase pumps in plasma membrane.     

The effects of G-CSF and naproxen sodium on the serum TGF-beta1 level and fracture healing in rat tibias

Local and systemic release of transforming growth factor beta 1 (TGF-beta1) is known to increase during the process of fracture healing and this cytokine stimulates bone healing. The majority of the non steroidal anti inflammatory drugs (NSAIDs) inhibit fracture healing. Granulocyte colony stimulating factor (G-CSF) is a hematopoietic growth factor that stimulates bone marrow. In this study, the effects of the NSAID naproxen sodium, G-CSF, and both of them in combination on the TGF-beta1 serum level in rats with tibia fractures were measured and fracture healing was evaluated by histopathologic and radiologic examination. The TGF-beta1 serum levels obtained on day one (24 h after fracture but before administration of naproxen or G-CSF) were found to be similar in all of the five groups (p > 0.05). At the end of the first week, TGF-beta1 levels were significantly lower in naproxen-treated rats than those of the other groups excluding control (p = 0.002). Similar changes in TGF-beta1 levels were found at the end of the second and fourth weeks. TGF-beta1 levels were significantly higher in G-CSF-treated rats at the end of the first, second and fourth weeks (p < 0.05). Fracture healing scores measured with histopathological and radiological methods were higher in G-CSF-treated rats than in naproxen-treated ones. When both naproxen and G-CSF were given, the scores resumed to normal. The results point to the negative effect of naproxen sodium on fracture healing is due to its decreasing effect on the level of TGF-beta1, which may be a new possible mechanism. Moreover, this negative effect can be inhibited by the use of G-CSF.     

Changes in the currents across sodium channels as affected by blood serum on cultured neuroblastoma cells

Adding of 5% bovine serum to internally perfused voltage-clamped serum deprived neuroblastoma cells rapidly stimulates transient sodium current. This stimulating effect is mainly due to the increase in the peak sodium conductance by almost 24 per cent, on the average. Besides that a modifying effect was observed resulting in the 6 mV shift of the sodium peak conductance curve towards more negative potentials and in the 5 mV shift of steady inactivation curve towards more positive ones. The sign of the latter shift was changed to the opposite under the action of serum thermally pretreated at 100 degrees C. This procedure led also to more than two fold lowering of the stimulating effect. Experiments with serum deprivation demonstrate different degrees of reversibility of the serum effects, the most reversible being the inactivation curve shift. EGF, insulin, dexamethasone, transferrin, ATP, serotonin and their combinations in physiological concentrations failed to give the typical whole serum effects. The serum is supposed to contain at least two active components of unknown nature, one of which being thermoresistant.