PURPOSE: Laparoscopic cholecystectomy (LC) is now a standard operation for benign gallbladder (GB) disease. However, previous upper abdominal surgery (UAS) has been regarded as a relative contraindication for LC. The purpose of this study was to examine the effects of history of upper abdominal surgery including gastrectomy on the operative and postoperative results of LC. METHODS: A total of 769 patients underwent LC between March 2008 and December 2015, and the surgical outcomes of 45 patients who had a history of UAS were retrospectively compared with those who did not. Twenty of 45 patients with a history of UAS received gastrectomy, and the remaining 25 received non-gastrectomy UAS. The degree of adhesion and clinical outcomes were further compared between these two groups. RESULTS: The patients with a history of UAS required placement of a greater number of trocars, longer operation time, longer duration of drainage insertion, and higher open conversion rate (4.4%) compared to patients with no history of UAS. However, there were no significant differences in postoperative hospital stay or complication rate between the two groups. In the UAS group, 93.3% of patients required adhesiolysis. There were no significant differences in clinical findings or perioperative outcomes between gastrectomy group and non-gastrectomy group. CONCLUSION: A history of UAS including gastrectomy increases the technical difficulty of LC as well as open conversion rate. However, LC can be a feasible and safe approach when performed with adequate methods.
Cholecystectomy, Laparoscopic* ; Drainage ; Gallbladder ; Gastrectomy* ; Humans ; Length of Stay ; Retrospective Studies ; Surgical Instruments

Mitochondria continuously fuse and divide to maintain homeostasis. An impairment in the balance between the fusion and fission processes can trigger mitochondrial dysfunction. Accumulating evidence suggests that mitochondrial dysfunction is related to neurodegenerative diseases such as Parkinson's disease (PD), with excessive mitochondrial fission in dopaminergic neurons being one of the pathological mechanisms of PD. Here, we investigated the balance between mitochondrial fusion and fission in the substantia nigra of a non-human primate model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. We found that MPTP induced shorter and abnormally distributed mitochondria. This phenomenon was accompanied by the activation of dynamin-related protein 1 (Drp1), a mitochondrial fission protein, through increased phosphorylation at S616. Thereafter, we assessed for activation of the components of the cyclin-dependent kinase 5 (CDK5) and extracellular signal-regulated kinase (ERK) signaling cascades, which are known regulators of Drp1(S616) phosphorylation. MPTP induced an increase in p25 and p35, which are required for CDK5 activation. Together, these findings suggest that the phosphorylation of Drp1(S616) by CDK5 is involved in mitochondrial fission in the substantia nigra of a non-human primate model of MPTP-induced PD.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Cyclin-Dependent Kinase 5 ; Cyclin-Dependent Kinases ; Dopaminergic Neurons ; Homeostasis ; Mitochondria ; Mitochondrial Dynamics ; Neurodegenerative Diseases ; Parkinson Disease ; Phosphorylation ; Phosphotransferases ; Primates ; Substantia Nigra

The function of microglia/macrophages after ischemic stroke is poorly understood. This study examines the role of microglia/macrophages in the focal infarct area after transient middle cerebral artery occlusion (MCAO) in rhesus monkeys. We measured infarct volume and neurological function by magnetic resonance imaging (MRI) and non-human primate stroke scale (NHPSS), respectively, to assess temporal changes following MCAO. Activated phagocytic microglia/macrophages were examined by immunohistochemistry in post-mortem brains (n=6 MCAO, n=2 controls) at 3 and 24 hours (acute stage), 2 and 4 weeks (subacute stage), and 4, and 20 months (chronic stage) following MCAO. We found that the infarct volume progressively decreased between 1 and 4 weeks following MCAO, in parallel with the neurological recovery. Greater presence of cluster of differentiation 68 (CD68)-expressing microglia/macrophages was detected in the infarct lesion in the subacute and chronic stage, compared to the acute stage. Surprisingly, 98~99% of transforming growth factor beta (TGFβ) was found colocalized with CD68-expressing cells. CD68-expressing microglia/macrophages, rather than CD206⁺ cells, may exert anti-inflammatory effects by secreting TGFβ after the subacute stage of ischemic stroke. CD68⁺ microglia/macrophages can therefore be used as a potential therapeutic target.
Brain ; Haplorhini ; Immunohistochemistry ; Infarction, Middle Cerebral Artery ; Inflammation ; Macaca mulatta ; Magnetic Resonance Imaging ; Microglia ; Middle Cerebral Artery ; Primates ; Stroke ; Transforming Growth Factor beta