Assessment of functional prognosis of anterior cruciate ligament reconstruction in athletes based on a body shape index.

BACKGROUND: A healthy body shape is essential to maintain athletes' sports level. At present, little is known about the effect of athletes' body shape on anterior cruciate ligament reconstruction (ACLR). Moreover, the relationship between body shape and variables such as knee joint function after operation and return to the field has not been well studied. AIM: To verify the relationship between a body shape index (ABSI) and the functional prognosis of the knee after ACLR in athletes with ACL injuries. METHODS: We reviewed 76 athletes with unilateral ACL ruptures who underwent ACLR surgery in the First Hospital of Shanxi Medical University between 2017 and 2020, with a follow-up period of more than 24 mo. First, all populations were divided into a High-ABSI group (ABSI > 0.835, n = 38) and a Low-ABSI group (ABSI < 0.835, n = 38) based on the arithmetic median (0.835) of ABSI values. The primary exposure factor was ABSI, and the outcome indicators were knee function scores as well as postoperative complications. The correlation between ABSI and postoperative knee function scores and postoperative complications after ACLR were analyzed using multifactorial logistic regression. RESULTS: The preoperative knee function scores of the two groups were similar. The surgery and postoperative rehabilitation exercises, range of motion (ROM) compliance rate, Lysholm score, and Knee Injury and Osteoarthritis Outcome Score of the two groups gradually increased, whereas the quadriceps atrophy index gradually decreased. The knee function scores were higher in the Low-ABSI group than in the High-ABSI group at the 24-mo postoperative follow-up (P < 0.05). In multifactorial logistic regression, ABSI was a risk factor of low knee joint function score after surgery, specifically low ROM scores (odds ratio [OR] = 1.31, 95% confidence interval [CI] [1.10-1.44]; P < 0.001), low quadriceps atrophy index (OR = 1.11, 95%CI [0.97-1.29]; P < 0.05), low Lysholm scores (OR = 2.34, 95%CI [1.78-2.94]; P < 0.001), low symptoms (OR = 1.14, 95%CI [1.02-1.34]; P < 0.05), low activity of daily living (OR = 1.34, 95%CI [1.18-1.65]; P < 0.05), low sports (OR = 2.47, 95%CI [1.78-2.84]; P < 0.001), and low quality of life (OR = 3.34, 95%CI [2.88-3.94]; P < 0.001). ABSI was also a risk factor for deep vein thrombosis of the lower limb (OR = 2.14, 95%CI [1.88-2.36], P < 0.05] and ACL recurrent rupture (OR = 1.24, 95%CI [0.98-1.44], P < 0.05) after ACLR. CONCLUSION: ABSI is a risk factor for the poor prognosis of knee function in ACL athletes after ACLR, and the risk of poor knee function after ACLR, deep vein thrombosis of lower limb, and ACL recurrent rupture gradually increases with the rise of ABSI.

Steroid receptor coactivator-3 differentially regulates the inflammatory response in peritoneal macrophages.

Steroid receptor coactivator-3 (SRC-3) is a transcriptional coactivator that plays an important role in the regulation of cytokine mRNA translation. In the present study, SCR-3 gene knockout mice were used to study the effects of SCR-3 on the regulation of the inflammatory response in peritoneal macrophages induced by lipopolysaccharides (LPS). Peritoneal macrophages (PMs) of SRC-3-/- mice showed a decrease in the release of TNF-α, IL-1ß and IL-6, and an increase in the release of IL-10. Furthermore, results of RT-PCR also showed that levels of TNF-α, IL-1ß and IL-6 mRNA expression were significantly lower, while the level of IL-10 mRNA expression was higher in the SRC-3-/- mice, compared to those of wild-type mice, following treatment with LPS (p < 0.01). In addition, western blotting revealed that: i) the extent of reduction of the glucocorticoid receptor in PMs from SRC-3-/- mice was significantly lower than that in wild-type mice (p < 0.01); ii) the extent of increase of AP-1 in PMS from SRC-3-/- mice was significantly lower than that in wild-type mice (p < 0.01); iii) the extent of increase of NF-κB p65 in PMs from SRC-3-/- mice was significantly higher than that in wild-type mice (p < 0.01). Collectively, our studies revealed that SRC-3 may play a key role in the maintenance of innate immunity. Furthermore, absence of the SRC-3 protein may result in the partial loss of inflammation and phagocytosis barrier function, including suppression of LPS-induced transcriptional activity, release of TNF-α, IL-1ß and IL-6, and obstruction of the function of phagocytes and elimination of bacteria, as well as their production.

Glycyrrhizin attenuates rat ischemic spinal cord injury by suppressing inflammatory cytokines and HMGB1.

AIM: To investigate the neuroprotective effect of glycyrrhizin (Gly) against the ischemic injury of rat spinal cord and the possible role of the nuclear protein high-mobility group box 1 (HMGB1) in the process. METHODS: Male Sprague-Dawley rats were subjected to 45 min aortic occlusion to induce transient lumbar spinal cord ischemia. The motor functions of the animals were assessed according to the modified Tarlov scale. The animals were sacrificed 72 h after reperfusion and the lumbar spinal cord segment (L2-L4) was taken out for histopathological examination and Western blotting analysis. Serum inflammatory cytokine and HMGB1 levels were analyzed using ELISA. RESULTS: Gly (6 mg/kg) administered intravenously 30 min before inducing the transient lumbar spinal cord ischemia significantly improved the hind-limb motor function scores, and reduced the number of apoptotic neurons, which was accompanied by reduced levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) in the plasma and injured spinal cord. Moreover, the serum HMGB1 level correlated well with the serum TNF-α, IL-1ß and IL-6 levels during the time period of reperfusion. CONCLUSION: The results suggest that Gly can attenuate the transient spinal cord ischemic injury in rats via reducing inflammatory cytokines and inhibiting the release of HMGB1.

Two clinically relevant pressures of carbon dioxide pneumoperitoneum cause hepatic injury in a rabbit model.

AIM: To observe the hepatic injury induced by carbon dioxide pneumoperitoneum (CDP) in rabbits, compare the effects of low- and high-pressure pneumoperitoneum, and to determine the degree of hepatic injury induced by these two clinically relevant CDP pressures. METHODS: Thirty healthy male New Zealand rabbits weighing 3.0 to 3.5 kg were randomly divided into three groups (n = 10 for each group) and subjected to the following to CDP pressures: no gas control, 10 mmHg, or 15 mmHg. Histological changes in liver tissues were observed with hematoxylin and eosin staining and transmission electron microscopy. Liver function was evaluated using an automatic biochemical analyzer. Adenine nucleotide translocator (ANT) activity in liver tissue was detected with the atractyloside-inhibitor stop technique. Bax and Bcl-2 expression levels were detected by western blotting. RESULTS: Liver functions in the 10 mmHg and 15 mmHg experimental groups were significantly disturbed compared with the control group. After CDP, the levels of alanine transaminase and aspartate transaminase were 77.3 ± 14.5 IU/L and 60.1 ± 11.4 IU/L, respectively, in the 10 mmHg experimental group and 165.1 ± 19.4 IU/L and 103.8 ± 12.3 IU/L, respectively, in the 15 mmHg experimental group, which were all higher than those of the control group (P < 0.05). There was no difference in pre-albumin concentration between the 10 mmHg experimental group and the control group, but the pre-albumin level of the 15 mmHg experimental group was significantly lower than that of the control group (P < 0.05). No significant differences were observed in the levels of total bilirubin or albumin among the three groups. After 30 and 60 min of CDP, pH was reduced (P < 0.05) and PaCO2 was elevated (P < 0.05) in the 10 mmHg group compared with controls, and these changes were more pronounced in the 15 mmHg group. Hematoxylin and eosin staining showed no significant change in liver morphology, except for mild hyperemia in the two experimental groups. Transmission electron microscopy showed mild mitochondrial swelling in hepatocytes of the 10 mmHg group, and this was more pronounced in the 15 mmHg group. No significant difference in ANT levels was found between the control and 10 mmHg groups. However, ANT concentration was significantly lower in the 15 mmHg group compared with the control group. The expression of hepatic Bax was significantly increased in the two experimental groups compared with the controls, but there were no differences in Bcl-2 levels among the three groups. Twelve hours after CDP induction, the expression of hepatic Bax was more significant in the 15 mmHg group than in the 10 mmHg group. CONCLUSION: A CDP pressure of 15 mmHg caused more substantial hepatic injury, such as increased levels of acidosis, mitochondrial damage, and apoptosis; therefore, 10 mmHg CDP is preferable for laparoscopic operations.

[Effects of different intraabdominal pressure of carbon dioxide pneumoperitoneum on hemorrheology and microcirculation in rabbits].

OBJECTIVE: To study effects of different intraabdominal pressure of carbon dioxide (Cq2) pneumoperitoneum on hemorrheology and microcirculation in rabbits. METHODS: Eighteen female healthy rabbits weighing 2.2 kg to 3.5 kg were randomly divided into three groups equally based on pneumoperitoneum pressure: 0 mmHg group (group I),10 mmHg group (group II) and 15 mmHg (group III). Each group received 1 h pneumoperitoneum under different pressure. Blood samples were taken at 5 min before CO2 pneumoperitoneum, at 30 and 60 min after pneumoperitoneum for the measurements of indexes of hemorrheology. Hemodynamics including heart rate (HR), mean arterial pressure (MAP) and the volume and velocity of the microcirculation of auricle were continuously monitored, such indexes were recorded at the related time. RESULTS: Afer pneumoperitoneum at 30 and 60 min, compared with group I, HR, MAP, the whole blood viscosity, the aggregation and rigid indexes of RBC were significantly raised in group II (P < 0.05), the deformability indexes of RBC, the volume and velocity of the microcirculation were markedly decreased (P < 0.05). Even more significant changes were observed in group III (P < 0.01). The plasma viscosity and the hematocrit changed little. CONCLUSION: After CO2 pneumoperitoneum, hemorrheology is decreased; Although HR, MAP are raised, the volume and velocity of the microcirculation are decreased.

Hepatic injury induced by carbon dioxide pneumoperitoneum in experimental rats.

AIM: To observe the hepatic injury induced by carbon dioxide pneumoperitoneum in rats and to explore its potential mechanism. METHODS: Thirty healthy male SD rats were randomly divided into control group (n = 10), 0 h experimental group (n = 10) and 1 h experimental group (n = 10) after sham operation with carbon dioxide pneumoperitoneum. Histological changes in liver tissue were observed with hematoxylin-eosin staining. Liver function was assayed with an automatic biochemical analyzer. Concentration of malonyldialdehyde (MDA) and activity of superoxide dismutase (SOD) were assayed by colorimetry. Activity of adenine nucleotide translocator in liver tissue was detected with the atractyloside-inhibitor stop technique. Expression of hypoxia inducible factor-1 (HIF-1) mRNA in liver tissue was detected with in situ hybridization. RESULTS: Carbon dioxide pneumoperitoneum for 60 min could induce liver injury in rats. Alanine aminotransferase and aspartate aminotransferase were 95.7 +/- 7.8 U/L and 86.8 +/- 6.9 U/L in 0 h experimental group, and 101.4 +/- 9.3 U/L and 106.6 +/- 8.7 U/L in 1 h experimental group. However, no significant difference was found in total billirubin, albumin, and pre-albumin in the three groups. In 0 h experimental group, the concentration of MDA was 9.83 +/- 2.53 micromol/g in liver homogenate and 7.64 +/- 2.19 micromol/g in serum respectively, the activity of SOD was 67.58 +/- 9.75 nu/mg in liver and 64.47 +/- 10.23 nu/mg in serum respectively. In 1 h experimental group, the concentration of MDA was 16.57 +/- 3.45 micromol/g in liver tissue and 12.49 +/- 4.21 micromol/g in serum respectively, the activity of SOD was 54.29 +/- 7.96 nu/mg in liver tissue and 56.31 +/- 9.85 nu/mg in serum, respectively. The activity of ANT in liver tissue was 9.52 +/- 1.56 in control group, 6.37 +/- 1.33 in 0 h experimental group and 7.28 +/- 1.45 (10(-9) mol/min per gram protein) in 1 h experimental group, respectively. The expression of HIF-1 mRNA in liver tissue was not detected in control group, and its optical density difference value was 6.14 +/- 1.03 in 0 h experimental group and 9.51 +/- 1.74 in 1 h experimental group, respectively. CONCLUSION: Carbon dioxide pneumoperitoneum during the sham operation can induce hepatic injury in rats. The probable mechanisms of liver injury include anoxia, ischemia reperfusion and oxidative stress. Liver injury should be avoided during clinical laparoscopic operation with carbon dioxide pneumoperitoneum.