Persistent cell volume reduction is a major hallmark of apoptosis. Recent studies have demonstrated that cell volume reduction is not a passive, secondary event of the apoptotic cell death process. Whole-cell shrinkage, termed apoptotic volume decrease (AVD), takes place soon after stimulation with apoptogen and precedes caspase activation, DNA and cell fragmentation in a variety of cell types including human epithelial cells. The AVD induction is the result of KCl efflux attained by activation of K(+) and Cl(-) channels. Inhibition of AVD induction leads to rescue of the cells from apoptosis. Since the AVD process is coupled to dysfunction of the regulatory volume increase (RVI), apoptotic cells undergo persistent cell shrinkage in human epithelial HeLa cells. When the RVI mechanism was impaired, hypertonic stress itself induced not only persistent cell shrinkage but also apoptotic cell death in HeLa cells. Even under normotonic apoptogen-free conditions, exposure of HeLa cells to Na(+)- or Cl(-)-deficient solution alone can bring about persistent cell shrinkage and thereafter apoptotic cell death. Thus, it is concluded that persistent cell shrinkage, which comprises AVD induction and RVI dysfunction, is a prerequisite to apoptosis induction in human epithelial cells.
Apoptosis ; Cell Size ; Epithelial Cells ; cytology ; HeLa Cells ; Humans ; Osmotic Pressure

Postoperative infections should be comprehensively controlled in the context of infection control, rather than as activities of individual surgeons. We started a surgical site infection (SSI) surveillance program in 2009 in which prophylactic measures for preventing SSIs were applied. These measures were as follows : 1) screening for nasal carriage of methicillin-resistant Staphylococcus aureus ; 2) dental checks and oral screening ; 3) antibiotic prophylaxis in the intra- and postoperative period ; 4) control of glucose levels to ≤160 mg/dl in the immediate postoperative period ; and 5) early removal of surgical drain. After the introduction of prophylactic measures, we reexamined SSI surveillance and added the following prophylactic measures at the beginning of 2011 : 6) data concerning SSI and compliance with prophylactic measures for all surgical and ward staff were published monthly, and the Infection Control Team (ICT) and surgeons performed weekly ward visits to assess SSIs ; 7) recommendations were made for wearing two pairs of gloves and surgical hoods to cover the hair, scalp, ears and neck ; and 8) collaboration with diabetologists was implemented to control glucose levels in diabetics. We compared incidences of SSI in cardiovascular surgery from the periods before (469 cases, Group B) and after (118 cases, Group A) introduction of the additional prophylactic measures. Clinical characteristics of patients in each group did not differ significantly. Operative time was significantly shorter in Group A (400±116 min) than in Group B (434±145 min). Compliance with antibiotic prophylaxis in the intraoperative period improved progressively from 93% in Group B to 99% in Group A. Compliance with control of glucose levels to ≤160 mg/dl on postoperative day 1 improved progressively from 71% in Group B to 81% in Group A. Duration of drain placement was significantly shorter in Group A (2.9±1.8 days) than in Group B (3.6±2.9 days). Incidence of SSI decreased significantly from 6.0% in Group B to 0.8% in Group A. Revision of preventive measures based on the results of surveillance and enhancement of cooperation between the ICT and surgeons could help to decrease the incidence of SSI.