A multivariate study of protective effects of Zn and Cu against nephrotoxicity induced by cadmium metallothionein in rats.

Factorial experimental design was used to study the protective effects of Zn and Cu on cadmium-metallothionein(CdMT)-induced nephrotoxicity in male Wistar rats. In the factorial design two levels of Zn (0 and 25 mg/kg body weight), two levels of Cu (0 and 12.5 mg/kg), and two levels of CdMT (0.1 and 0.4 mg of Cd/kg) were used as varied factors. The factorial design was complemented with a center point with all three variables at an intermediate setting, i.e., Zn at 12.5 mg/kg, Cu at 6.25 mg/kg, and CdMT at 0.25 mg Cd/kg. Each of the nine combinations of settings was administered to one of nine groups with six rats in each. Zn and Cu were injected sc 24 hr prior to the injection of CdMT. The concentrations of protein and Ca in urine and Ca in renal cortex were used as effects. The relationship between the experimental design settings and the effects were modeled with multiple regression. The multiple regression analysis revealed that for the high dose of CdMT (i) the enhanced values of protein in urine caused by CdMT injection could be more efficiently reduced by Zn than by Cu, and (ii) excessive Ca in urine and renal cortex could be more efficiently reduced by Cu than by Zn. No significant synergism or antagonism between Cu and Zn was found. These models can be used to estimate the dose levels of Zn and Cu which will reduce the toxic effects of CdMT. The treatment of 20.4 mg/kg Zn, for example, will reduce the effects of 0.4 mg Cd/kg as CdMT on protein in urine, and 2.8 mg/kg Cu will reduce the Ca in urine to the levels of those caused by 0.25 mg Cd/kg (no Zn and Cu). Similarly, the effect of 0.4 mg Cd/kg on Ca level in renal cortex can be reduced to that of 0.28 mg Cd/kg as CdMT by 7.98 mg Cu/kg, which is three times as efficient as Zn. The obtained results might be of importance in understanding the mechanism of cadmium toxicity and the potential risk to the health of the population exposed to cadmium occupationally or environmentally.     

HTLV-1 associated T cell lymphoma in South East Asia: case report and family study.

Geographic clustering of human T cell lymphoma/leukaemia virus type 1 (HTLV-1) infection is well recognised, particularly in south western Japan, parts of West and Central Africa, the south eastern United States and the Caribbean islands. Sporadic cases have been reported in many other parts of the world. The first case of HTLV-1 associated leukaemia/lymphoma (ATLL) in South East Asia is reported. Contact tracing showed a high incidence of carriers among the relatives.     

Tongqiao Huoxue Tang and Buyang Huanwu Tang for Treatment of Vascular Dementia -A report of 36 Cases

To study the effects of Tongqiao Huoxue Tang (通窍活血汤) and Buyang Huanwu Tang (补阳还五汤) onvascular dementia (VaD), 36 VaD patients in thetreatment group were treated with the two decoctions,which were compared with 28 cases in a controlgroup treated with Duxil.     

Effect of shenmai Injection on SIL-2R NK and LAK cells of patients with advanced carcinoma

Serum interleukin-2 receptor (sIL-2R) level, activities of natural killer cell (NK) and lymphokine activated killer (LAK) cells were determined in 60 patients with advanced carcinoma (AC) before and after treatment with Shenmai Injection (SMI), forty healthy persons were taken as non-carcinoma control (NC). The results showed that: Serum sIL-2R level in AC were much higher than those in NC (P<0.05) and activities of NK and LAK cells in AC were much lower than those in NC (P<0.05) before treatment. There was no significant difference among gastric, colonic and lung cancer (P>0.05). After treatment with SMI, it was found that the level of sIL-2R in all patients were obviously lowered (P<0.05) while the activities of NK and LAK cells were signifficantly higher than that prior the treatment (P<0.05). Relevancy was not found between sIL-2R and NK, LAK cells. These data suggested that the immune function was compromised in AC, and SMI has a wide effect of immuno-regulation.     

Organic anion transport in HepG2 cells: absence of the high-affinity, chloride-dependent transporter.

In previous studies, we identified a 55 kD organic anion-binding protein in liver cell sinusoidal plasma membrane subfractions. Other investigators identified another 55 kD bromosulfophthalein/bilirubin binding protein on the surface of rat hepatocytes and HepG2 cells and suggested that this protein served as a transporter for these ligands. In this study, transport of 35S-sulfobromophthalein by the human hepatoma cell line, HepG2, was quantified in the presence and absence of bovine serum albumin to further clarify the possible function of these plasma membrane binding proteins. In contrast to results in normal rat hepatocytes, virtually no uptake of 35S-sulfobromophthalein by HepG2 cells in the presence of bovine serum albumin was found. In the absence of albumin, HepG2 cells expressed temperature-dependent uptake of 35S-sulfobromophthalein. However, the high-affinity Cl(-)-dependent sulfobromophthalein transport that characterizes normal rat hepatocytes was absent, as indicated by an approximately 95-fold lower affinity and 170-fold higher capacity of HepG2 cells for sulfobromophthalein compared with previous results with rat hepatocytes. These results suggest that 55 kD sulfobromophthalein/bilirubin-binding protein on the liver cell surface differs from organic anion-binding protein and is not responsible for sulfobromophthalein extraction in the presence of albumin, although it may play some role in lower affinity transport by cells. Immunoblot analysis and metabolic labeling of HepG2 cells demonstrated synthesis of organic anion-binding protein. However, light microscopic immunocytochemistry and immunoprecipitation of surface iodinated rat hepatocytes and HepG2 cells with antibody to a recombinant organic anion-binding protein fusion protein indicated absence of organic anion-binding protein on the surface of HepG2 cells.(ABSTRACT TRUNCATED AT 250 WORDS)     

脊髓萎缩（附2例报告）

本文报告了两例脊髓萎缩，并结合文献复习讨论了该病的好发部位、病因、临床表现、诊断和治疗。脊髓萎缩的病因多为继发性，也可为特发性。根据临床表现结合脊髓ＣＴ造影及ＭＲＩ检查，可以明确诊断。