Objective To investigate the clinical effect of laparoscopic gallbladder surgery in 76 cases underwent appendectomy.Methods A retrospective analysis was conducted in 76 cases of gallbladder appendectomy (the observation group) and 23 cases over the same period received gallbladder laparotomy (the control group).The treatment effect,operative time,blood loss,postoperative discharge,hospitalization time and VAS pain score and so on were observed.Results The patients were successfully operated,17.1％ in the observation group used sedatives,fever 14.5％,antibiotic usage time was (3.5 ± 1.5)d,mean operative time was (51.5 ± 10.5)min,blood loss was (40.5 ± 10.5) ml,postoperative exhaust time was (13.5 ± 3.5) h,average length of stay was (4.5 ± 2.5) d,VAS pain score was (3.01 ± 0.55) points.Those in control group were 78.3％,65.2％,(6.5 ± 1.5) d,(65.5 ± 15.5) min,(90.5 ± 20.5) ml,(16.5 ± 4.5) h,(7.5 ± 2.5) d,(5.84 ± 0.82) points,the differences were statistically significant(x2 =30.7,23.5,t=19.9,10.7,32.1,7.46,11.9,42.0,all P＜0.01).Conclusion Laparoscopic cholecystectomy appendectomy surgical has less trauma,it can reduce patients'pain and shorten recovery time,which has positive clinical significance.

BACKGROUND:Since damage control theory system was founded, this theory in the orthopedics has been applied gradualy, especialy in elderly hip fracture surgery that reduces the negative impacts due to inflammatory responses. OBJECTIVE:To explore whether flurbiprofen axetil can reduce inflammatory responses in rats with hip fractures based on the damage control theory. METHODS: Forty-nine healthy Sprague-Dawley rats weighing 250-300 g were randomly divided into four groups:control group (n=7), immediate internal fixation group (n=14), flurbiprofen axetil group (n=14), damage control group (n=14). Rats in the control group moved freely in the cages. Rats in the other three groups were intraperitonealy injected with composite anesthetics to make unilateral hip fracture models, and then respectively given internal fixation immediately after fracture, flurbiprofen axetil injection and delayed internal fixation, and delayed internal fixation. Levels of serum C-reactive protein, interleukin-6 and tumor necrosis factor-α were determined and analyzed before fixation, immediately after internal fixation and at 4, 8, 12, 24, 48 hours after internal fixation in different groups. RESULTS AND CONCLUSION:Postoperative serum levels of C-reactive protein, interleukin-6, tumor necrosis factor-αwere al increased in different groups. The level of C-reactive protein reached the peak at 24 hours after internal fixation. Flurbiprofen axetil injection had no significant influence on the level of C-reactive protein in rats with delayed internal fixation (P=0.51). Interleukin-6 levels were stil increased at 48 hours after internal fixation, but flurbiprofen axetil reduced the level of interleukin-6 significantly in rats with delayed internal fixation (P < 0.01). The tumor necrosis factor-α level peaked at 4 hours after internal fixation, and flurbiprofen axetil injection could significantly reduce the level of tumor necrosis factor-α in rats with delayed internal fixation (P < 0.01). These findings indicate that flurbiprofen axetil as a new non-steroidal anti-inflammatory drug can reduce the inflammatory response in rats with hip fractures after internal fixation, and also can aleviate the inflammatory response of rats undergoing delayed operation under the guidance of damage control theory.

Vascular cognitive impairment (VCI), caused by cerebrovascular dysfunction, severely impacts the quality of life in the elderly population, yet effective therapeutic approaches remain limited. Mitophagy, a selective mitochondrial quality-control mechanism, has emerged as a critical focus in neurological disease research. Accumulating evidence indicates that mitophagy modulates oxidative stress, neuroinflammation, and neuronal apoptosis. Key signaling pathways associated with mitophagy—including PINK1/Parkin, BNIP3/Nix, FUNDC1, PI3K/Akt/mTOR, and AMPK—have been identified as potential therapeutic targets for VCI. This review summarizes the mechanistic roles of mitophagy in VCI pathogenesis and explores emerging therapeutic strategies targeting these pathways, aiming to provide novel insights for clinical intervention and advance the development of effective treatments for VCI.