PURPOSE: Laparoscopic cholecystectomy has been performed even in case of acute cholecystitis and GB empyema with increasing experience of laparoscopic surgery. Many previous studies has been recommended early laparoscopic cholecystectomy in acute cholecystitis. METHODS: From February, 1997 to January, 2000, 364 patients were attempted to laparoscopic cholecystectomy and 71 patients of them were attempted to laparoscopic cholecystectomy due to acute cholecytitis. They were divided into 4 groups based on the time of operation form the onset of symptom. These groups were compared in conversion rate and postoperative clinical outcomes, such as operation time, time of bowel movement, starting diet, starting soft diet and discharge. The affecting factors on conversion were analyzed (age, sex, fever, murphy sign, accompanying pancreatitis, SGOT/SGPT, alkaline phosphatase, GB wall thickening, WBC count). RESULTS: Among 71 patients who were attempt to laparoscopic cholecystectomy in acute cholecystitis, 20 patients (28.1%) required converting to open surgery. There were no statistically significant difference in clinical outcomes and conversion rate between four groups (p>0.568). In univariate analyis, high frequency of conversion to open surgery in acute cholecystitis was observed in male (p=0.012). CONCLUSION: Even though conversion rate to open surgery is still high in acute cholecystitis, the time of laparoscopic surgery in acute cholecystits does not affect on the conversion rate and postoperative clinical outcomes. Considering of the hospital stay and its related economic problems, laparoscopic cholecystectomy should be attempted as soon as possible without hesitation. It may be due to advanced laparoscopic techniques and experiences.
Alkaline Phosphatase ; Cholecystectomy, Laparoscopic* ; Cholecystitis, Acute* ; Conversion to Open Surgery ; Diet ; Empyema ; Fever ; Humans ; Laparoscopy ; Length of Stay ; Male ; Pancreatitis

PURPOSE: In non-excitable cells, which include parotid and pancreatic acinar cells, Ca(2+) entry is triggered via a mechanism known as capacitative Ca(2+) entry, or store-operated Ca(2+) entry. This process is initiated by the perception of the filling state of endoplasmic reticulum (ER) and the depletion of internal Ca(2+) stores, which acts as an important factor triggering Ca(2+) entry. However, both the mechanism of store-mediated Ca(2+) entry and the molecular identity of store-operated Ca(2+) channel (SOCC) remain uncertain. MATERIALS AND METHODS: In the present study we investigated the Ca(2+) entry initiation site evoked by depletion of ER to identify the localization of SOCC in mouse parotid and pancreatic acinar cells with microfluorometeric imaging system. RESULTS: Treatment with thapsigargin (Tg), an inhibitor of sarco/endoplasmic reticulum Ca(2+)-ATPase, in an extracellular Ca(2+) free state, and subsequent exposure to a high external calcium state evoked Ca(2+) entry, while treatment with lanthanum, a non-specific blocker of plasma Ca(2+) channel, completely blocked Tg-induced Ca(2+) entry. Microfluorometric imaging showed that Tg-induced Ca(2+) entry started at a basal membrane, not a apical membrane. CONCLUSION: These results suggest that Ca2+ entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC.
Animals ; Calcium/*metabolism ; Calcium Channels/drug effects/metabolism ; Cells, Cultured ; Endoplasmic Reticulum/drug effects/*metabolism ; Mice ; Mice, Inbred ICR ; Microscopy, Fluorescence ; Pancreas/cytology/drug effects/*metabolism ; Parotid Gland/cytology/drug effects/*metabolism ; Thapsigargin/pharmacology

Holoprosencephaly is a rare malformation complex or development defect including different degrees of incomplete cleavages of the embryonic prosencephalon and varying degrees of the midface defects, resulting from the defect of prechordal mesoderm, migrating forward into the area anterior to the notochord during the third week of fetal development. Early antenatal diagnosis of holoprosencephaly is important to find out its severity, to predict its prognosis, and to determine proper management according to its prognosis and severity. The possibility of early antenatal diagnosis of holoprosencephaly by ultrasound has been suggested, but occasionally missed and rarely confirmed. We present one case of lobar holoprosencephaly, diagnosed postnatally and one case of alobar holoprosencephaly, diagnosed antenatally in our hospitals.
Fetal Development ; Holoprosencephaly* ; Mesoderm ; Notochord ; Prenatal Diagnosis ; Prognosis ; Prosencephalon ; Ultrasonography

PURPOSE: The sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), encoded by ATP2A2, is an essential component for G-protein coupled receptor (GPCR)-dependent Ca(2+) signaling. However, whether the changes in Ca(2+) signaling and Ca(2+) signaling proteins in parotid acinar cells are affected by a partial loss of SERCA2 are not known. MATERIALS AND METHODS: In SERCA2(+/-) mouse parotid gland acinar cells, Ca(2+) signaling, expression levels of Ca(2+) signaling proteins, and amylase secretion were investigated. RESULTS: SERCA2(+/-) mice showed decreased SERCA2 expression and an upregulation of the plasma membrane Ca(2+) ATPase. A partial loss of SERCA2 changed the expression level of 1, 4, 5-tris-inositolphosphate receptors (IP(3)Rs), but the localization and activities of IP3Rs were not altered. In SERCA2(+/-) mice, muscarinic stimulation resulted in greater amylase release, and the expression of synaptotagmin was increased compared to wild type mice. CONCLUSION: These results suggest that a partial loss of SERCA2 affects the expression and activity of Ca(2+) signaling proteins in the parotid gland acini, however, overall Ca(2+) signaling is unchanged.
Amylases/metabolism ; Animals ; Blotting, Western ; Calcium/metabolism ; Calcium Signaling/drug effects/genetics/*physiology ; Carbachol/pharmacology ; Immunohistochemistry ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Mice ; Mice, Knockout ; Parotid Gland/*metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics/*metabolism ; Signal Transduction/drug effects/genetics/physiology

Synaptotagmin is a Ca2+ sensing protein, which triggers a fusion of synaptic vesicles in neuronal transmission. Little is known regarding the expression of Ca2+ - dependent synaptotagmin isoforms and their contribution to the release of secretory vesicles in mouse and rat parotid acinar cells. We investigated a type of Ca2+ - dependent synaptotagmin and Ca2+ signaling in both rat and mouse parotid acinar cells using RT-PCR, microfluorometry, and amylase assay. Mouse parotid acinar cells exhibited much more sensitive amylase release in response to muscarinic stimulation than did rat parotid acinar cells. However, transient [Ca2+]i increases and Ca2+ influx in response to muscarinic stimulation in both cells were identical, suggesting that the expression or activity of the Ca2+ sensing proteins is different. Seven Ca2+ - dependent synaptotagmins, from 1 to 7, were expressed in the mouse parotid acinar cells. However, in the rat parotid acinar cells, only synaptotagmins 1, 3, 4 and 7 were expressed. These results indicate that the expression of Ca2+ - dependent synaptotagmins may contribute to the release of secretory vesicles in parotid acinar cells.
Synaptotagmins/*metabolism ; Signal Transduction ; Rats ; Protein Isoforms/metabolism ; Parotid Gland/cytology/*metabolism ; Muscarinic Agonists/pharmacology ; Mice ; Exocytosis/drug effects/physiology ; Carbachol/pharmacology ; Calcium/metabolism/*physiology ; Animals ; Amylases/secretion