Traditional mineral medicine realgar and Realgar-Indigo naturalis formula potentially exerted therapeutic effects by altering the gut microbiota.

Introduction: Realgar has a long history ofuse in traditional medicines. However, the mechanism through which Realgar or Realgar-Indigo naturalis formula (RIF) exert therapeutic effects is only partially understood. Methods: In this study, 60 feces and 60 ileum samples from rats administered with realgar or RIF were collected to examine the gut microbiota. Results: The results showed that realgar and RIF influenced different microbiota in both feces and ileum. Compared with realgar, RIF at low dosage (0.1701 g/3 ml) significantly increased the microbiota diversity. LEfSe and random forest analyses showed that the bacterium Bacteroidales was significantly altered after RIF administration, and it was predicted that these microorganisms contribute to the inorganic arsenic metabolic process. Discussion: Our results suggest that realgar and RIF may exert their therapeutic effects through influencing microbiota. The low dose of RIF had greater effects on increasing the diversity of microbiota, and Bacteroidales in feces might participate in the inorganic arsenic metabolic process to exert therapeutic effects for realgar.

[Clinical Analysis of Serum Calcium Level in 86 Cases of Newly Diagnosed Multiple Myeloma].

OBJECTIVE: To investigate the serum calcium level in 86 patients with newly diagnosed multiple myeloma (MM) and its correlation with clinical features. METHODS: The clinical data of 86 patients with newly diagnosed multiple myeloma in our hospital from 2009 to 2016 were retrospectively analyed. Clinical data of sex, age, hemoglobin, albumin, globulin, creatinine, uric acid, serum phosphorus, ß2-microglobulin, immunophenotyping and disease staging were collected. After the serum calcium level was corrected, the patients were grouped into low serum calcium (<2.20 mmol/L), normal serum calcium (2.20-2.60 mmol/L) and high serum calcium (>2.60 mmol/L). The correlation between the clinical characteristics and the serum calcium level was analysed, the clinical characteristics between the low and non-low calcium group were compared. RESULTS: The number of cases in low, normal and high serum cnlcium groups before correction was 58 (67.4%), 18 (20.9%) and 10 (11.6%) respactively, while the number of cases in 3 group after correction was 34 (39.5%), 36 (41.9%) and 16 (18.6%) respectively. The age, globulin, creatinine, uric acid and serum phosphorus levels were positively correlated with serum calcium level in patients with multiple myeloma, while the sex, hemoglobin,albumin and ß2-microglobulin levels did not correlated with serum calcium level. There was significant difference in the age, globulin, creatinine and serum phosphorus between low calcium and non-low calcium group (P<0.05). However the differences of sex, hemoglobin, albumin, uric acid, ß2-microglobulin, immunophenotyping and clinical stage were not statistically significant (P>0.05). CONCLUSION: Multiple myeloma patients suffered from both hypercalcemia and hypocalcemia, and the incidence of hypocalcemia is not low. The levels of serum calcium in patients with multiple myeloma correlate with age, globulin, creatinine, uric acid, serum phosphorus level and other factors, thus it is necessary to correct the level of ionized calcium with physiological activity.

Effects of Clostridium difficile toxin A on K562/A02 cell proliferation, apoptosis and multi-drug resistance.

The aim of the present study was to investigate the cytotoxic effect and multi-drug resistance (MDR) of Clostridium difficile toxin A (TcdA) on K562/A02 cells, and understand its underlying molecular pathways. K562/A02 cells were treated with TcdA at different concentrations for 24, 48 and 72 h, and the inhibition effect and drug resistance of TcdA on K562/A02 cell proliferation was assessed by methyl thiazolyl tetrazolium colorimetric assay. Furthermore, cell cycle-apoptosis was analyzed by flow cytometry, P-glycoprotein (P-gp) expression was determined by western blot analysis and caspase-3 activity was measured using a caspase-3 activity kit. TcdA inhibited K562/A02 cell proliferation in a time- and dose-dependent manner. The inhibition rate of K562/A02 cells reached 8.76±0.76, 28.55±0.43, 47.89±0.27, 58.08±0.06 and 57.70±0.79% following treatment with 50, 100, 200, 400 and 800 ng/ml TcdA, respectively, for 24 h. K562/A02 cells in the G0/G1 phase increased and cells in the S phase decreased following treatment with TcdA (P<0.05), and the apoptotic rates in the 200 and 400 ng/ml concentration groups were 14.05 and 22.89%, respectively. In addition, TcdA (50 ng/ml) significantly inhibited the proliferation of K562/A02 cells and reduced the half maximal inhibitory concentration of these drugs in combination with chemotherapy drugs. The reversal folds were 3.09, 2.89 and 2.79, respectively. Furthermore, TcdA treatment was associated with the upregulation of P-gp in K562/A02 cells, and caspase-3 activity was observed to increase in K562/A02 cells following TcdA treatment, when compared with untreated controls (P<0.05). These findings suggested that TcdA may be able to inhibit K562/A02 cell growth, induce cell apoptosis by decreasing P-gp levels and caspase-3 activation, and partially reverse MDR. Further studies are required to evaluate the potential of TcdA as a candidate for the chemotherapy of hematologic malignancies.