Objective:A C57/BL6 mouse model of traumatic temporomandibular joint ankylosis (TTMJA) was established through composite trauma to lay the foundation for studying the pathophysiology of TTMJA.Methods:This study was conducted from January 2024 to February 2025. Forty-two 4-weeks old C57/BL6 mice, numbered 1 to 42, are randomly assigned to a control group ( n=21) and an experimental group ( n=21) using a computer-generated random number sequence. The experimental group undergoes modeling surgery on the left temporomandibular joint (TMJ), while the control group is routinely raised without special treatment. At 12 weeks post-surgery, the TMJ complex of both groups is assessed via body weight and mouth opening measurements, gross observation, micro-CT, and histological staining to evaluate model establishment. Results:At 12 weeks post-operation, in the experimental group, the body weight of mice [(27.75±1.08) g] did not show a significant difference compared with that of the control group [(30.80±0.29) g]( t=0.54, P=0.610). The maximum vertical passive mouth opening [(1.70±0.26) mm] in the experimental group was significantly lower than that in the control group [(3.43±0.21) mm]( t=8.92, P<0.001). Gross observation indicated that the right TMJ structure of the experimental-group mice was normal, while irregular hyperplasia occurred in the left TMJ complex. Micro-CT revealed that at 12 weeks post-operation, the right joint structure of the experimental-group mice was normal, with regular condyles and glenoid fossae. On the left side, a large amount of bone hyperplasia occurred on the lateral side of the joint in the condyles and glenoid fossae, forming two irregular bone masses, and there was an uncalcified radiolucent zone between the bone masses. In histological staining, no new cartilage or bone tissue was observed in the left joint space of the control-group mice, and the articular disc structure was normal. In the experimental-group mice, obvious new cartilage and calcified bone tissue were visible on the lateral side of the left joint space. A bone bridge was formed between the condyles and glenoid fossae, the articular disc structure disappeared, and bony ankylosis occurred. Conclusions:In this experiment, a TTMJA model of C57/BL6 mice was initially established by removing the articular disc and damaging part of the fibrous cartilage of the glenoid fossae and condyles, providing an experimental platform for further research on the pathogenesis of TTMJA.

Objective:A C57/BL6 mouse model of traumatic temporomandibular joint ankylosis (TTMJA) was established through composite trauma to lay the foundation for studying the pathophysiology of TTMJA.Methods:This study was conducted from January 2024 to February 2025. Forty-two 4-weeks old C57/BL6 mice, numbered 1 to 42, are randomly assigned to a control group ( n=21) and an experimental group ( n=21) using a computer-generated random number sequence. The experimental group undergoes modeling surgery on the left temporomandibular joint (TMJ), while the control group is routinely raised without special treatment. At 12 weeks post-surgery, the TMJ complex of both groups is assessed via body weight and mouth opening measurements, gross observation, micro-CT, and histological staining to evaluate model establishment. Results:At 12 weeks post-operation, in the experimental group, the body weight of mice [(27.75±1.08) g] did not show a significant difference compared with that of the control group [(30.80±0.29) g]( t=0.54, P=0.610). The maximum vertical passive mouth opening [(1.70±0.26) mm] in the experimental group was significantly lower than that in the control group [(3.43±0.21) mm]( t=8.92, P<0.001). Gross observation indicated that the right TMJ structure of the experimental-group mice was normal, while irregular hyperplasia occurred in the left TMJ complex. Micro-CT revealed that at 12 weeks post-operation, the right joint structure of the experimental-group mice was normal, with regular condyles and glenoid fossae. On the left side, a large amount of bone hyperplasia occurred on the lateral side of the joint in the condyles and glenoid fossae, forming two irregular bone masses, and there was an uncalcified radiolucent zone between the bone masses. In histological staining, no new cartilage or bone tissue was observed in the left joint space of the control-group mice, and the articular disc structure was normal. In the experimental-group mice, obvious new cartilage and calcified bone tissue were visible on the lateral side of the left joint space. A bone bridge was formed between the condyles and glenoid fossae, the articular disc structure disappeared, and bony ankylosis occurred. Conclusions:In this experiment, a TTMJA model of C57/BL6 mice was initially established by removing the articular disc and damaging part of the fibrous cartilage of the glenoid fossae and condyles, providing an experimental platform for further research on the pathogenesis of TTMJA.

Objective To observe the dynamic changes of myocardial structure and dysfunction during post-resuscitation period in order to establish a rat mode of post-resuscitation myocardial dysfunction after cardiac arrest resulted from electric stimulation-induced ventricular fibrillation (VF) and cardiopulmonary resuscitation (CPR).Methods A total of 40 male Sprague-Dawley (SD) rats were randomly (random number) assigned into post-resuscitation (PR) 4 h,PR 12 h,PR 24 h,PR 72 h and sham groups.VF was induced by an alternating electric current delivered to the right ventricular endocardium and untreated for 8 min.Biphasic waveform defibrillation was attempted and mechanical ventilation was synchronized after 6 min of CPR.Myocardial function was assessed with serum myocardial enzyme activity,echocardiography,mitochondrial respiratory function and histopathologic findings at different intervals.Results Thirty-two animals were successfully resuscitated with restoration of spontaneous circulation (ROSC) in 86％ (32/37) rats.Compared with sham group,severe systolic and diastolic heart failure were found at 4 h after ROSC and then gradually improved without significant difference (P ＞0.05) in ejection fraction at PR 72 h after ROSC was found,whereas thickened ventricular wall and increased myocardial performance index as well as interstitial proliferation were observed at 72 h after ROSC.Conclusions A rat model of post-resuscitation myocardial dysfunction after cardiac arrest resulted from electric stimulation-induced VF and CPR was successfully established.

Objective To investigate the risk factors of posttraumatic hydrocephalus (PTH) in patients with moderate to severe traumatic brain injury (TBI).Methods Aretrospective study was conducted for 183 patients with moderate to severe TBI (125 males,58 females;6-91 years of age,mean 48.23 years).According the presence of PTH,the patients were allocated into PTH group (n =34) and non-PTH group (n =149).Risk factors of PTh were assessed by univariate and logistic regression analysis,including gender,age,injury types,injury severity,intraventricular hemorrhage,subarachnoid hemorrhage,midline shift,subdural effusion,therapeutic strategies and skull defect.Association between the boundaries of skull defect and PTH was determined.Results Between-group differences were not significant regarding age,gender,injury types and intraventricular hemorrhage (P ＞ 0.05),but differed significantly in injury severity,subarachnoid hemorrhage,midline shift,subdural effusion,craniectomy and skull defect (P ＜ 0.05).Further Logistic regression analysis confirmed subarachnoid hemorrhage (OR =6.169),interhemispheric subdural effusion (OR =31.743),and unilateral (OR =17.602) and bilateral (OR =30.567) skull defects were risk factors of PTH.Of the patients with unilateral skull defect following decompressive craniectomy,the inferior limit ≤ 10 mm from the zygomatic arch also played a role in the development of PTH (OR =5.500,P ＜ 0.05).Conclusions Subarachnoid hemorrhage,interhemispheric subdural effusion and skull defect are risk factors of PTH.Unilateral skull defects with the inferior limit too close to the zygomatic arch can predispose to the development of PTH.

Objective　To investigate the effects of isocarbophos, a new and highly effective organophosphorus pesticide on the membranes of keratinocytes. Methods　The epidermic cells of human skin cultured in the medium were adopted as a biological material.The activity of lactate dehydrogenase (LDH) was used as an indicator. We tested the activities of LDH and alkaline phosphatase (ALP) in the medium in different isocarbophos dosage conditions. Results　It was found that the activity of LDH in the medium decreased with the increase of isocarbophos dosage. The LDH activities of the dosage groups were statistically different from those of the positive and negative groups. The ALP activities were of no significant difference between the groups. Conclusion　The above findings reveal that isocarbophos does not damage the membranes of keratinocytes directly, howerer it inhibits the LDH of human skin keratinocytes; thus it is suggested that isocarbophos like most organophosphorus pesticides used widely can pass through the intact human skin and poison the body before the skin is damaged. Therefore, protection during work hours is of paramount importance.