Emergency general surgery in a public hospital in Malaysia.

INTRODUCTION: Patients undergoing emergency general surgery (EGS) are at risk for death and complications. Information on the burden of EGS is critical for developing strategies to improve the outcomes. METHODS: In this retrospective cohort study, medical records of all general surgical operations in a public hospital were reviewed for the period 1st January 2017 to 31st December 2017. Data on patient demographics, operative workload, case mix, time of surgery and outcomes were analysed. RESULTS: Of the 2960 general surgical operations that were performed in 2017, 1720 (58.1%) of the procedures were performed as emergencies. The mean age for the patients undergoing emergency general surgical procedures was 37.9 years (Standard Deviation, ±21.0), with male preponderance (57.5%). Appendicitis was the most frequent diagnosis for the emergency procedures (43%) followed by infections of the skin and soft tissues (31.6%). Disorders of the colon and rectum ranked as the third most common condition, accounting for 6.7% of the emergency procedures. Majority of emergency surgery (59.3%) took place after office hours and on weekends. Post-operative deaths and admissions to critical care facilities increased during EGS when compared to elective surgery, p<0.01. CONCLUSIONS: EGS constitutes a major part of the workload of general surgeons and it is associated significant risk for death and post-operative complications. The burden of EGS must be recognised and patient care systems must evolve to make surgery safe and efficient.

[Apoptosis resistance and its reversal in harringtonine resistant cell line].

Harringtonine (HT), a domestic antitumor drug extracted from Cephalotaxus hainanensis Li showed high chemotherapeutic efficacy on human acute granulocytic leukemia and acute myelocytic leukemia in clinics. Apoptosis of HL-60 cells can be induced by HT effectively; but for cells resistant to harringtonine, apoptosis can not be induced, even if the drug (HT) concentration is over 100 times of IC50 value. Although apoptosis occurred when its multidrugs resistance had been reversed by verapamil, compared with sensitive HL-60 cells, the time at which apoptosis happened delayed and the drug dosage increased. All these suggest that apoptotic resistance might be one of the marks of drug resistance in tumor cells, and apoptosis related factors could play a role in the formation of multidrug resistance.

[Retardation of human drug-resistant HL-60 cell in G1 phase and induction of sensitive cell to apoptosis by cyclosporine A].

To further study the relationship between resistance to apoptosis and drug resistance in harringtonine-resistant HL-60 cells (HR20), cyclosporine A (CsA) 20, 10 micrograms.ml-1 was shown to induce the sensitive HL-60 cells to apoptosis, showing a typical DNA "ladder" band. But the same concentrations of CsA retarded the HR20 cells in G1 phase and could not induce the cells to apoptosis. The cellular daunorubicin accumulation increased when HR20 cells were treated with low concentration of CsA and the reversal of drug resistance by CsA was unrelated to the retardation of cell cycle progression. High phosphorylation of about 50 kDa protein occured when HR20 cells were treated with CsA 10 micrograms.ml-1. The results domonstrate that cyclosporine A retarded the harringtonine-resistant HL-60 cells in G1 phase but induced HL-60 cells to apoptosis, and the retardation was unrelated to drug resistance.

[Effects of differentiation status on apoptosis of human leukemia HL60 cells].

The effects of differentiation of human leukemia HL60 cells on harringtonine(Har) and camptothecin(Cam) induced apoptosis(in these cells) were studied. When treated with phorbol 12-myriate, 13-acetate 16 nmol.L-1 for 24 h, the HL60 cells differentiated into monocyte/macrophage cells and were arrested at G1 phase. The differentiated cells were shown to be resistant to the Har and Cam induced apoptosis, but showed no change of expression of c-myc gene. HL60 cells incubated in 1.4% dimethyl sulfoxide for 48 h differentiated into granulocyte cells and were also gene arrested at G1 phase. The differentiated cells became resistant to the apoptosis induced by Cam, but not that by Har, and expression of c-myc decreased drastically in the differentiated cells. The results indicate that the differentiated status of human leukemia HL60 cells apparently affected the apoptosis induced by harringtonine and camptothecin, but it was irrelevant to the change of the expression of c-myc gene.

Pancreatic islets express a Ca2+-independent phospholipase A2 enzyme that contains a repeated structural motif homologous to the integral membrane protein binding domain of ankyrin.

Pancreatic islets express a Ca2+-independent phospholipase A2 (CaI-PLA2) activity that is sensitive to inhibition by a haloenol lactone suicide substrate that also attenuates glucose-induced hydrolysis of arachidonic acid from islet phospholipids and insulin secretion. A cDNA has been cloned from a rat islet cDNA library that encodes a protein with a deduced amino acid sequence of 751 residues that is homologous to a CaI-PLA2 enzyme recently cloned from Chinese hamster ovary cells. Transient transfection of both COS-7 cells and Chinese hamster ovary cells with the cloned islet CaI-PLA2 cDNA resulted in an increase in cellular CaI-PLA2 activity, and this activity was susceptible to inhibition by haloenol lactone suicide substrate. The domain of the islet CaI-PLA2 from amino acid residues 150-414 is composed of eight stretches of a repeating sequence motif of approximately 33-amino acid residues in length that is highly homologous to domains of ankyrin that bind both tubulin and integral membrane proteins, including several proteins that regulate ionic fluxes across membranes. These findings complement previous pharmacologic observations that suggest that CaI-PLA2 may participate in regulating transmembrane ion flux in glucose-stimulated beta-cells.

Resistance to apoptosis of harringtonine-resistant HL60 cells induced by tetrandrine.

AIM: To study the mechanism of resistance to apoptosis in the harringtonine (Har)-resistant HL60 cells with tetrandrine (Tet). METHODS: Growth inhibition, flow cytometry, DNA agarose gel electrophoresis, protein phosphorylation, and RNA dot hybridization. RESULTS: The resistant cells had no cross resistance to Tet. Tet induced the sensitive but not the Har-resistant HL60 cells to apoptosis. The high phosphorylation of protein < 30 kDa occurred when the resistant cells were treated with Tet. Tet and Har increased the expression of c-myc mRNA in the sensitive HL60 cells. The expression of c-myc mRNA in the resistant cells was obviously decreased and almost not changed in treatment with Tet and Har. CONCLUSION: Tet induced the sensitive but not the Har-resistant HL60 cells to apoptosis, and the resistance to apoptosis induced by Tet was associated with the high protein phosphorylation and reduction of the expression of c-myc mRNA.