The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

The intestine and liver share a unique regenerative property that sets them apart from other mammalian visceral organs. The intestinal epithelium exhibits rapid renewal, making it one of the fastest renewing tissues in humans. Under physiological conditions, intestinal stem cells within each intestinal crypt continuously differentiate into the different types of intestinal epithelial cells to maintain intestinal homeostasis. However, when exposed to tissue damage or stressful conditions such as inflammation, intestinal epithelial cells in the gastrointestinal tract exhibit plasticity, allowing fully differentiated cells to regain their stem cell properties. Likewise, hepatic epithelial cells possess a remarkable regenerative capacity to restore lost liver mass through proliferationmediated liver regeneration. When the proliferation-mediated regenerative capacity is impaired, hepatocytes and biliary epithelial cells (BECs) can undergo plasticity-mediated regeneration and replenish each other. The transition of mammalian liver progenitor cells to hepatocytes/BECs can be observed under tightly controlled experimental conditions such as severe hepatocyte injury accompanied by the loss of regenerative capacity. In this review, we will discuss the mechanism by which cellular plasticity contributes to the regeneration process and the potential therapeutic implications of understanding and harnessing cellular plasticity in the gut and liver.

Purpose: To evaluate the prevalence of dry eye symptoms after endoscopic dacryocystorhinostomy (EDCR) for patients with primary acquired nasolacrimal duct obstruction (PANDO) combined with dry eye syndrome. Methods: The patients diagnosed with PANDO combined with dry eye syndrome who underwent EDCR were divided into two groups according to the questionnaire about dry eye symptoms after surgery. The medical records were retrospectively analyzed. Before and after surgery, we compared the tear meniscus height, tear breakup time, and the presence of corneal punctuate epithelial erosion. The level of dry eyes of patients after surgery was assessed by using the Korean guidelines for the diagnosis of dry eye. Results: At 6 months after EDCR, the proportion of patients with dry eye symptoms was 30% in a total of 80 patients. The duration of epiphora and tear breakup time after EDCR were higher in the group without dry eye symptoms and the proportion of eyes with corneal punctuate epithelial erosion after EDCR was higher in the group with dry eye symptoms. About 15% of total patients started treatment with a dry eye of level 2 or higher. Conclusions About 15% of patients who underwent EDCR for PANDO combined with dry eye syndrome developed significant dry eye syndrome after surgery. The short onset of epiphora was associated with the development of the dry eye symptoms. Therefore, it is necessary to evaluate dry eye syndrome before surgery, and surgeons should be careful about this.

Background: Studies have reported favorable outcomes using the paratricipital approach for fixation of distal humeral intra-articular fractures. However, literature evaluating the clinical results of the approach remains limited. The objective of this study was to compare clinical outcomes between type 13C2 and type 13C1 distal humeral fractures after open reduction and internal fixation performed using the same approach and same type of plate. Methods: A total of 52 adults with type 13C1 or 13C2 distal humeral fractures were treated surgically at our institution during 2006 to 2018. We retrospectively analyzed data from 29 of these patients (19 with type 13C1 fractures and 10 with 13C2 fractures) who met the inclusion criteria. All subjects were followed for a minimum of 2 years postoperatively. Clinical and radiologic results were analyzed to determine differences in outcomes between the two types of fractures. Clinical results were evaluated using elbow range of motion (ROM), Mayo Elbow Performance Score (MEPS), and Quick Disabilities of the Arm, Shoulder and Hand (Q-DASH) score. Alignment, fracture union, and presence of posttraumatic arthritis were evaluated radiologically. Results: The patients’ mean age was 51 years, and the mean duration of follow-up was 29 months. Mean ROM was 129.5° ± 21.5° in the type 13C1 group and 123.0° ± 20.6° in the 13C2 group (p = 0.20). Mean Q-DASH score was 12.6 ± 11.7 in the 13C1 group and 16.2 ± 19.8 in the 13C2 group (p = 0.60). Mean MEPS was 92.9 ± 8.5 in the 13C1 group and 85.0 ± 14.1 in the 13C2 group (p = 0.09). Carrying angle did not differ significantly between the 13C1 and 13C2 groups. No patient in either group exhibited nonunion or posttraumatic arthritis. Conclusions Although the paratricipital approach has the disadvantage of limited visualization of articular surfaces, there were no differences in surgical outcomes between type 13C1 and type 13C2 distal humeral fractures after fixation using this approach.Thus, surgeons may need to consider using the paratricipital approach for open reduction and internal fixation of 13C2 distal humeral fractures.

Background: The rupture of the central slip of an extensor tendon of a finger causes a boutonniere (or buttonhole) deformity, characterized by pathologic flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Currently, there are no standard treatment guidelines for this deformity. This study aimed to report clinical results of surgery to correct chronic boutonniere deformity. Methods: This retrospective case series was conducted between January 2010 and December 2018 and only 13 patients with trauma-induced chronic deformity were included. After excision of elongated scar tissue, a direct anatomic end-to-end repair using a loop suture technique with supplemental suture anchor augmentation was conducted. Total active motion was assessed before and after surgery and self-satisfaction scores were collected from phone surveys. Results: All patients presented with Burton stage I deformities defined as supple and passively correctable joints. The initial mean extension lag of the PIP joint (43.5°) was improved by an average of 21.9° at the final follow-up (p < 0.001). The mean hyperextension of the DIP joint averaged 19.2° and improved by 0.8° flexion contracture (p < 0.001). The average total active motion was 220.4° (range, 160°–260°). Based on the Souter’s criteria, 69.2% (9/13) of the patients had good results. Only 1 patient reported fair outcome and 23.1% (3/13) reported poor outcome. The average Strickland formula score was 70 (range, 28.6–97.1). In total, 10 patients (77%) had excellent or good results. Of 10 patients contacted by phone, self-reported satisfaction score was very satisfied in 2, satisfied in 3, average in 3, poor in 1, and very poor in 1. Three patients reported a relapse of the deformity during range of motion exercises, 1 of whom underwent revision surgery. One patient complained of PIP joint flexion limitation, and 2 complained of DIP joint flexion limitation at final follow-up. Conclusions In chronic boutonniere deformity, central slip reconstruction with anchor suture augmentation can be an easily applicable surgical option, which offers fair to excellent outcome in 77% of the cases. The risk of residual extension lag and recurrence of deformity should be discussed prior to surgery.

Background: The rupture of the central slip of an extensor tendon of a finger causes a boutonniere (or buttonhole) deformity, characterized by pathologic flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Currently, there are no standard treatment guidelines for this deformity. This study aimed to report clinical results of surgery to correct chronic boutonniere deformity. Methods: This retrospective case series was conducted between January 2010 and December 2018 and only 13 patients with trauma-induced chronic deformity were included. After excision of elongated scar tissue, a direct anatomic end-to-end repair using a loop suture technique with supplemental suture anchor augmentation was conducted. Total active motion was assessed before and after surgery and self-satisfaction scores were collected from phone surveys. Results: All patients presented with Burton stage I deformities defined as supple and passively correctable joints. The initial mean extension lag of the PIP joint (43.5°) was improved by an average of 21.9° at the final follow-up (p < 0.001). The mean hyperextension of the DIP joint averaged 19.2° and improved by 0.8° flexion contracture (p < 0.001). The average total active motion was 220.4° (range, 160°–260°). Based on the Souter’s criteria, 69.2% (9/13) of the patients had good results. Only 1 patient reported fair outcome and 23.1% (3/13) reported poor outcome. The average Strickland formula score was 70 (range, 28.6–97.1). In total, 10 patients (77%) had excellent or good results. Of 10 patients contacted by phone, self-reported satisfaction score was very satisfied in 2, satisfied in 3, average in 3, poor in 1, and very poor in 1. Three patients reported a relapse of the deformity during range of motion exercises, 1 of whom underwent revision surgery. One patient complained of PIP joint flexion limitation, and 2 complained of DIP joint flexion limitation at final follow-up. Conclusions In chronic boutonniere deformity, central slip reconstruction with anchor suture augmentation can be an easily applicable surgical option, which offers fair to excellent outcome in 77% of the cases. The risk of residual extension lag and recurrence of deformity should be discussed prior to surgery.

Purpose: Soft tissue defects of the distal lower extremity are commonly accompanied by a fracture of the lower extremities. Theses defects are caused by the injury itself or by complications associated with surgical treatment of the fracture, which poses challenging problem. The reverse superficial sural artery flap (RSSAF) is a popular option for these difficult wounds. This paper reviews these cases and reports the clinical results. Materials and Methods: Between August 2003 and April 2018, patients who were treated with RSSAF for soft tissue defects of the lower third of the leg and ankle related to a fracture were reviewed. A total of 16 patients were involved and the mean follow-up period was 18 months. Eight cases (50.0%) of the defects were due to an open fracture, whereas the other eight cases (50.0%) were postoperative complication after closed fracture. The largest flap measured 10×15 cm2 and the mean size of the donor sites was 51.9 cm2. The flap survival and postoperative complications were evaluated. Results: All flaps survived without complete necrosis or failure. One case with partial necrosis of the flap was encountered, but the wound healed after debridement and repair. One case had a hematoma with a pseudoaneurysmal rupture of the distal tibial artery. On the other hand, the flap was intact and the wound healed after arterial ligation and flap advancement. A debulking operation was performed on three cases for cosmetic reasons and implant removal through the flap was performed in three cases. No flap necrosis was encountered after these additional operations. Conclusion RSSAF is a relatively simple and safe procedure for reconstructing soft tissue defects following a fracture of the lower extremity that does not require microsurgical anastomosis. This can be a useful treatment option for soft tissue defects on the distal leg, ankle, and foot.

BACKGROUND: Since the first report of a rapidly resolved subdural hemorrhage (SDH) in 1986, few additional case reports have been presented in the literature. CASE REPORT: An 82-year-old female patient presented with a SDH over the left convexity. The SDH was removed via catheter drainage through a burr hole trephination. Post-operative computed tomography (CT) following 300 mL drainage from the chronic SDH demonstrated a newly developed SDH along the right convexity. A follow-up CT performed 2 hours later revealed an unexpected significant resolution of the acute SDH. CONCLUSION: The spontaneous resolution of acute SDH is believed to result from redistribution by washout of the hematoma by cerebrospinal fluid dilution. However, its exact pathophysiology is not well understood. When surgical evacuation is considered in acute SDH, conservative management should also be considered because spontaneous resolution of hemorrhage remains a possibility.
Aged, 80 and over ; Catheters ; Cerebrospinal Fluid ; Drainage ; Female ; Follow-Up Studies ; Hematoma ; Hematoma, Subdural ; Hematoma, Subdural, Chronic ; Hemorrhage ; Humans ; Trephining