BACKGROUND: It is controversial whether the delay of surgery for acute appendicitis by physician results in higher morbidity. Our present study explores this problem of physician delay on the postoperative outcome of patients with acute appendicitis. MATERIAL AND METHODS: Among 432 patients admitted for the presumptive diagnosis of acute appendicitis between Jan., 1995 and Dec., 1997, 358 patients with pathologically proven acute appendicits were analyzed. Physician delay from the hospital admission to the surgery was evaluated in relation to the stage of the disease at operation and postoperative outcome. RESULTS: Postoperative complications occurred signifficantly higher in advanced appendicitis group, than in simple appendicitis group. Postoperative oral consumption started significantly later and hospital days are significantly prolonged in those group. Both patient and physician delays significantly affect the stage of the disease. The finding that physician delay correlated with the stage, however, was denied by multivariate analysis. CONCLUSION: On the contrary to the patient delay, physician delay does not affect the stage of the acute appendicitis nor lead to increased incidence of postoperative complication. Physician delay to clarify the diagnosis is a reasonable strategy and it does not affect the outcome adversely.
Appendicitis* ; Diagnosis ; Humans ; Incidence ; Multivariate Analysis ; Postoperative Complications

The authors have experienced a case of histiocytosis-X. A 7-year-old male patient had three tender masses, one on the right parietal region, another on the left parietal region, the other on the left occipital region and revealed exophthalmus on his left side. Plain skull films showed multiple punched out skull defects and on lumbar spine films, collapse of body of second lumbar vertebra was detected. Among the masses, the largest right parietal one was excised totally. The final diagnosis revealed histiocytosis-X on pathologic basis and he was given subsequent chemotheraphy.
Child ; Diagnosis ; Histiocytosis, Langerhans-Cell* ; Humans ; Male ; Rabeprazole ; Skull ; Spine

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

Anterior cruciate ligament (ACL) rupture leads to weakened quadriceps muscle strength and a decline in proprioception, impairing the neuromuscular control of the lower extremities. ACL reconstruction, aimed at addressing such structural and functional instability, has become a primary treatment method for young and active patients. Consequently, there have been significant advancements in surgical techniques, resulting in improved clinical outcomes. However, achieving successful outcomes after ACL reconstruction is not solely dependent on the surgery itself; pre- and postoperative rehabilitation and management are equally crucial. A well-designed functional recovery program based on medical evidence before and after ACL reconstruction plays a vital role in restoring function to preinjury levels. The process of the functional recovery program, from presurgery to sports return, should adhere to certain principles. These principles involve prompt and accurate clinical diagnosis and patient classification after injury, systematic programs addressing joint swelling and inflammation control, reduction of arthrogenic muscle inhibition, restoration of range of motion, muscle strength recovery, and proprioception restoration. Postoperatively, it is essential to go beyond traditional methods (such as range of motion restoration and muscle strengthening) by implementing a functional recovery program that includes enhancement of proprioception and neuromuscular control system from the early stages, considering the biological healing response of the graft. This comprehensive approach is vital for achieving optimal outcomes in the recovery of function after ACL reconstruction.

n patients who have undergone knee joint surgery or suffer from osteoarthritis, weakened quadriceps muscle strength is often observed. This can lead to various pathological issues in the long term, such as abnormal gait and persistent knee pain. Due to the need to protect against pain or surgical site complications, high-intensity exercise is often restricted for most patients with muscle atrophy in the knee joint due to surgery or osteoarthritis or surgery. To overcome this challenge, various methods are being attempted, including exercise combined with neuromuscular electrical stimulation, blood flow restriction (BFR) exercise, and biofeedback exercise. Recently, BFR exercise has garnered attention in line with these strategic trends. Applying low-intensity BFR exercise to patients who have undergone anterior cruciate ligament reconstruction surgery or suffer from knee joint osteoarthritis, most studies report improvements in strength, muscle mass, and functional enhancement of the knee joint. Compared to non-BFR high-intensity exercise, it has been reported that increases in maximal strength and muscle mass are similar, but pain reduction is superior with BFR exercise. Engaging in low-intensity BFR exercise for a sufficient duration can minimize the risk of injury associated with high-intensity exercise while maximizing the exercise’s effectiveness, leading to symptom improvement and enhancement of knee joint function. Furthermore, when conducted according to specified manuals, the likelihood of cardiovascular imbalance, muscle damage, thrombosis, and embolism due to BFR is low, making it a safe rehabilitation method.