[Clinical application of self-made drainage tubes in different layers of soft tissue for negative-pressure wound therapy in 33 patients].

From January 2014 to June 2018, 28 patients with different types of deep soft tissue injury or infection were admitted to the Affiliated Jiangyin Hospital of Medical College of Southeast University; 5 patients were admitted to the Zhengzhou First People's Hospital. There were 24 males and 9 females, aged 18-89 (40±20) years. Disposable suction tubes with holes cut on side walls were used as self-made drainage tubes. The authors placed the self-made drainage tubes on different deep soft tissue layers and wound surfaces after debridement. The effective drainage sections of the wound surface drainage tubes were wrapped with silver ion antimicrobial functional active dressings. Bio-permeable membrane was used to close the operative area. The drainage tubes in the deep layer of wound and wound surface were connected in parallel by a tee and connected to wall-hanging medical negative-pressure suction device to conduct negative-pressure wound treatment at -20.0 to -10.6 kPa. The deep drainage tubes were usually removed or changed 4 or 5 days after surgery.The drainage tubes in the wound surface were synchronously replaced when removing or replacing he drainage tubes in the deep layer of wound. On 4 to 15 days after surgery, the deep drainage tubes were removed. On 8 to 25 days after surgery, the wound surface drainage tubes were removed. Then the treatment was changed to a conventional dressing change until the wounds were completely healed or the wound bed was ready for skin grafts or tissue flaps. The indwelling time of deep drainage tubes in this group of patients was (6.2±2.8) days, and the indwelling time of wound surface drainage tubes was (12.0±3.0) days. The wound healing time was (22±5) days, the hospital stay time was (29±7) days, and wound bacteria were reduced from 6 species and 11 strains before treatment to 3 species and 4 strains after treatment. No adverse events such as wound bleeding, irritative pain, and chronic sinus occurred during treatment. Twenty-three patients were followed up for 13 to 28 months, no treatment-related complications were observed.

Protein kinase C in the promyelocytic leukemia cell differentiation of granulocytes.

When the leukemia cells in 14 patients with acute promyelocytic leukemia (APL) were induced by all-trans retinoic acid (RA) treatment, the activity of protein kinase C (PKC) increased with the differentiation. In the control cells, the activity of PKC was only 47 +/- 39.3 pmol.mg-1/min, while it was 149.3 +/- 150.1 pmol.mg-1/min after differentiation. There were 90.1 +/- 7.2% promyelocytes in the control group, and 8.9 +/- 5.6% in the induction group. Therefore, we think that there is a close correlation between PKC and the differentiation of promyelocytic leukemia cells.

Studies on the relationship between protein kinase C and differentiation of human promyelocytic leukemia cells induced by retinoic acid.

We studied the differentiation of acute promyelocytic leukemia (APL) cells in 14 patients with APL. After the induction by retinoic acid (RA) the mature cells rose to 60 +/- 11.8% compared to 0.7 +/- 1% of the control, while the promyelocytes declined to 8.7 +/- 6.4% (93.3 +/- 5.6% in the control group). Protein kinase C (PKC) activity was significantly increased to 149.3 +/- 156.2 pmol/mg per min compared to 47 +/- 40.9 of the control (p less than 0.01). In HL-60 cells, the activity of PKC increased also from 52.3 +/- 35 to 129.2 +/- 64.6 pmol/mg per min (n = 10, p less than 0.01) after the induction of differentiation with RA. If the leukemia cells were pretreated with a kind of PKC inhibitor such as trifluoperazine, the increase of PKC activity was inhibited, and the rate of nitroblue tetrazolium reduction decreased from 89.9 +/- 7.7% to 62 +/- 25% (n = 6, p less than 0.01) and the mature cells reduced from 63.1 +/- 11.7% to 19.7 +/- 12.2% (p less than 0.01). We presumed that the activity of PKC is closely related to the differentiation of human promyelocytic leukemia cells induced by all-trans-retinoic acid.