Acta cirurgica brasileira最新文献

Purpose: To compare and evaluate the radiologic, clinical, and histopathologic results of the treatment methods applied in diaphyseal tibial fractures.

Methods: A complete tibial fracture was created in the tibial diaphysis in each rabbit. Experimentally generated fracture fragments were fixed by intramedullary pinning. In the control group (group I), the bone fracture area was left to heal without any treatment technique. Group II received low-energy laser therapy once daily to the surgical side for 30 days; group III, autologous bone marrow aspirated from the left proximal tibia; group IV, a combination of bone marrow obtained by aspiration and synthetic β-tricalcium phosphate (β-TCP); and in group V, a platelet-rich fibrin (PRF) membrane obtained from the central auricular artery was applied to the fracture side.

Results: In the X-ray analysis, it was determined that group IV had the fastest score increase, while group I had the lowest scores. In group IV, no lameness that persisted until the end of the study was observed in any rabbit. When the histopathological scores of the different groups were examined, it was seen that the lowest score belonged to group I, and the highest score was in group IV.

Conclusion: The highest rate of new bone formation and bone regeneration was achieved when the combination of aspirated bone marrow and β-TCP granules was applied. The experimental group with PRF membrane application exhibited the least osteogenic characteristics among all experimental groups.

Purpose: To examine the protective effect of alpinumisoflavone against streptozotocin (STZ)-induced gestational diabetes mellitus (GDM) in female rats and explored the underlying mechanisms.

Methods: Female rats were used in this study, and intraperitoneal administration of STZ (55 mg/kg) was used to induce diabetes. Body weight, blood glucose level, fetuses, placental weight, and placental index were estimated. Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed. The levels of resistin, glycated hemoglobin (HbA1c), hepatic glycogen, free fatty acid (FFA), adiponectin, serum C-peptide, leptin, visfatin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), lipids, oxidative stress, inflammatory cytokines, and other parameters were estimated. mRNA expression was estimated in the pancreatic tissue.

Results: Alpinumisoflavone treatment significantly (p < 0.001) enhanced body weight and fetuses and decreased placental weight and placental index. Alpinumisoflavone treatment significantly (p < 0.001) decreased blood glucose levels (BGL) and improved plasma insulin levels. Alpinumisoflavone treatment significantly (p < 0.001) suppressed the glucose and insulin levels in the OGTT and ITT. Alpinumisoflavone treatment significantly (p < 0.001) altered the levels of resistin, HbA1c, hepatic glycogen, FFA, Adiponectin, serum C-peptide, leptin, visfatin, ICAM-1, and VCAM-1; lipid parameters; oxidative stress parameters; inflammatory cytokines and inflammatory parameters, viz., cyclooxygenase-2 (COX-2), and nuclear kappa B factor (NF-κB). Alpinumisoflavone treatment significantly (p < 0.001) altered the mRNA expression levels of Toll-like receptor 4, nuclear kappa B factor65 (NF-κB65), NOD-, LRR-, pyrin domain-containing protein 3 (NLRP3), MyD88, SREBP-1, stearoyl-CoA desaturase-1 (SCD1), FAS, and ACC.

Conclusion: Alpinumisoflavone has a protective effect against STZ-induced GDM via alteration of the TLR4/MyD88/NF-κB signaling pathway.

Purpose: To investigate the optimal therapeutic sequence of rhGM-CSF combined with hypofractionated radiotherapy (HFRT) in treating mouse pancreatic cancer (PC) and explore the mechanisms.

Methods: A PC-bearing model was established. The antitumor effects were observed under rhGM-CSF, HFRT, rhGM-CSF + HFRT, rhGM-CSF&HFRT, and HFRT + rhGM-CSF treatments. Tumor histopathological changes were examined using hematoxylin and eosin (H&E) staining. FCM was employed to detect calreticulin (CRT), mDCs, CD4+, and CD8+ T cells. Enzyme-linked immunosorbent assay (ELISA) was used to measure HMGB1, adenosine triphosphate (ATP), interleukin- (IL)-2, IL-4, IL-8, IL-10, IL-12, IFN-γ, tumor necrosis factor (TNF)-α, and iNOS levels. IF staining was performed to detect CD31 and α-smooth muscle actin, and immunohistochemistry was used to detect vascular endothelial growth factor (VEGF), soluble VEGF receptor-1 (sVEGFR-1), hypoxia-inducible factor- (HIF)-1α, and HIF-2α expression.

Results: HFRT + rhGM-CSF inhibited tumor growth, promoted tumor necrosis, and increased inflammatory cell infiltration. This regimen also significantly enhanced immunogenic cell death by inducing CRT exposure and the release of HMGB1 and ATP. Furthermore, HFRT + rhGM-CSF markedly increased proportions of mDCs, CD4+ T cells, and CD8+ T cells, and upregulated expressions of IL-2, IL-8, IL-12, IFN-γ, TNF-α, and iNOS, but not IL-4 and IL-10. Additionally, rhGM-CSF synergized with HFRT to promote the normalization of blood vessels in the PC.

Conclusion: HFRT followed by rhGM-CSF had the best efficacy in PC, and the molecular mechanism may be related to immunogenic cell death.

Purpose: To analyze the geographical distribution of patients treated at a burn treatment unit (BTU) in Catanduva, São Paulo, Brazil, and examine the relationship between geographic and clinical variables.

Methods: This is a cross-sectional study that analyzed patients hospitalized for burns between January 2018 and May 2022. Data were obtained from medical records and included patients' residence city, age, and percentage of total body surface area burned (%TBSA). The data were processed using QGIS and R, and travel distances and times were calculated. Statistical analyses included bivariate and correlation tests.

Results: The total of 1,164 patients were analyzed. Most of them resided outside Catanduva, totaling 277 cities. The average distance was 179.37 km, and the average travel time was 140.94 minutes. Patients from Catanduva had an average age of 35.55 years old, and the average %TBSA was 12.15. Patients from outside Catanduva were significantly younger and had a higher %TBSA than the local patients. A weak but significant negative correlation was found between patient age and distance to the BTU (ρ = -0.14, p < 0.05), while %TBSA showed a weak positive correlation with travel distance (ρ = 0.21, p < 0.05). No significant differences were observed between the pre- and pandemic periods.

Conclusion: This study highlights regional differences in specialized burn care access and may inform policy aimed at reducing care disparities.

Purpose: To investigate the potential pleiotropic effects of liraglutide (LG), a glucagon-like-peptide-1 analog, on gastric ulcer prevention in rats with diabetes induced by streptozotocin (STZ).

Methods: We randomly divided 63 male Wistar rats into seven groups. STZ was administered intraperitoneally (IP) to the animals in the diabetic control (group STZ), diabetic control + indomethacin (INDO) (group STZI), STZ + INDO + omeprazole (group OMP), STZ + INDO + LG (0.2 mg/kg) (group 0.2LG), and STZ + INDO + LG (0.4 mg/kg) group (group 0.4LG). We administered OMP IP to group OMP, 0.2 mg/kg LG to group 0.2LG SC, 0.4 mg/kg LG to group 0.4LG SC, normal saline to non-diabetic control (sham group), group STZ, non-diabetic control + INDO (group KI), and group STZI SC. INDO was administered to the animals in groups KI, STZI, OMP, 0.2LG, and 0.4LG by gavage. Then, the caspase-3, epidermal growth factor (EGF), vascular endothelial growth factor-A (VEGF-A), prostaglandin E2 (PGE2), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), superoxide dismutase-1 (SOD-1), glutathione (GSH), and malondialdehyde (MDA) levels were studied.

Results: LG prevented INDO-induced ulcers and decreased apoptosis in the stomach tissue. It increased the SOD-1, GSH, EGF, VEGF-A, and PGE2 levels, and reduced the MDA, IL-6, and TNF-α levels. The anti-ulcer effect of LG was lower, but close to that of OMP.

Conclusion: The antioxidant, anti-inflammatory, and anti-apoptotic effects of LG, its ability to regulate EGF, VEGF-A, and PGE2 levels, and its capacity to reduce blood glucose levels in diabetic rats may contribute to its anti-ulcer effect.

Purpose: To evaluate whether hematemesis is associated with increased morbidity and mortality for upper gastrointestinal bleeding.

Methods: A retrospective cohort study was conducted at a quaternary university hospital from January 2022 to September 2024. Adults presenting with upper gastrointestinal bleeding, confirmed by endoscopy, were included. We excluded patients with terminal disease, patients who refused to receive blood products, and trauma. The main outcomes were all-cause mortality, need for orotracheal intubation, emergency blood transfusion, need for re-endoscopy, and length of hospital and intensive care unit (ICU) stays.

Results: A total of 69 patients (65% male, mean age 58 years) were included. Hematemesis was associated with a higher need for emergency blood transfusions (73% vs. 23%; odds ratio - OR = 8.82, 95% confidence interval - 95%CI 2.44-31.94, p = 0.001), longer hospital (12 vs. 6 days; mean difference - MD = 6.02, 95%CI 2.39-9.64, p = 0.001) and ICU stays (7.7 vs. 3.2 days; MD = 4.5, 95%CI 1.73-7.26, p = 0.002). Data were sparse and imprecise on all-cause mortality, orotracheal intubation, and the need for re-endoscopy.

Conclusion: Hematemesis is associated with higher transfusion requirements and longer hospital and ICU stays. These findings highlight the potential predictive value of hematemesis in acute upper gastrointestinal bleeding.

Purpose: This study analyzed the protective effects of enoxaparin in rat uteruses by exposing the uterus to experimental ischemia-reperfusion injury.

Methods: Thirty female rats were homogenized by weight and cycle and divided into three groups: a control group, an ischemia-reperfusion (I/R) group, and an ischemia-reperfusion plus enoxaparin (I/R+E) group. An experimental uterine I/R model was established in the I/R and I/R+E groups. Unlike I/R group, all rats in the I/R+E group received subcutaneous enoxaparin at 0.5 mg/kg 2 hours before ischemia. In histopathological analysis, endometrial glandular and endo/myometrial stromal changes were scored according to the histopathological scoring system. Biochemically, catalase (CAT), superoxide dismutase (SOD) enzyme activities, and malondialdehyde (MDA) levels were measured in uterine tissues.

Results: In histopathological analysis, all of the control group's scores were lower than those of the other groups, except for necrosis (p 0.05). There was no significant improvement in the glandular and stromal changes between I/R and I/R+E (p 0.05). However, the I/R+E group showed significantly increased SOD and CAT activities and decreased MDA levels compared to the I/R group (p = 0.000).

Conclusion: Although enoxaparin did not significantly improve histopathological injury, its potent antioxidant effects suggest a protective role against oxidative stress in uterine I/R injury.

Purpose: To evaluate the protective effect of Caesalpinia sappan and spirulina against gastritis and determine changes in the expression of CD8, CD68, and major histocompatibility complex (MHC) molecules.

Methods: Gastritis was induced in 24 female Wistar albino rats on the first day using ethanol. The treatment groups were given C. sappan (250 mg/kg) and spirulina (400 mg/kg) using oral gavage for five days. Blood and stomach tissue samples of the mice were analyzed.

Results: Caesalpinia sappan and spirulina increased CD8 and CD68 expression and tumor necrosis factor-alpha levels thereby decreasing the severity of inflammation. It was found that they simultaneously decreased MHC I and MHC II expressing cells, increased superoxide dismutase levels, whereas malondialdehyde, and myeloperoxidase levels decreased in the treatment group.

Conclusion: This study revealed that C. sappan and spirulina can protect gastric mucosa by reducing oxidative stress and inflammation.

Purpose: To investigate the protective effects of fisetin on ovarian ischemia-reperfusion injury in rats, focusing on the modulation of the TLR4-MyD88-TRAF6 signaling pathway.

Methods: Wistar rats randomly divided into different groups received oral administration of fisetin (5, 10 and 15 mg/kg). Body weight and ovary weight were measured. Hormones, hematological, antioxidant, cytokines, inflammatory and apoptosis parameters were assessed. Histological and histopathologic evaluations were conducted on ovary tissue. Different mRNA expressions were estimated.

Results: Dose dependent treatment significantly improved body and ovary weight along with alteration in hematological parameters such as red blood cells, white blood cells, hemoglobin, platelet, lymphocyte; antioxidant parameters, including malonaldehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase; cytokines viz., tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-18 (IL-18); inflammatory parameters such as cyclooxynase-2, inducible nitric oxide synthetase (iNOS), prostaglaindin, nuclear kappa B factor (NF-κB), C reactive protein and apoptosis parameters, including Bcl-2, Bax, and caspase-3. Fisetin treatment significantly (p < 0.001) altered the mRNA expression of TNF-α, IL-6, IL-1β, IL-10, Bax, Bcl-2, caspase-3, toll-like receptor 4, myeloid differentiation primary response protein 88, tumor necrosis factor receptor-associated factor 6, endothelial nitric oxide synthase, iNOS, NF-κB, inhibitor of kappaB kinase alpha, heme oxygenase-1, and nuclear factor erythroid 2-related factor 2. Fisetin treatment altered the hemorrhage, vascular proliferation, polymorphonuclear leukocyte, edema, vascular congestion, and apoptosis.

Conclusion: Fisetin ameliorated the ovary injury against ovarian ischemia-reperfusion via conquering TLR4-MyD88-TRAF6 signaling pathway.

Purpose: Mitophagy is an important process in brain damage, and the precise impact on a traumatic brain injury (TBI) model remains unclear. AMP-activated protein kinase (AMPK) regulates mitochondrial homeostasis and mitophagy, which are closely related to the remission of early brain injury. This study sought to explore the mechanism behind AMPK/optic atrophy 1 (OPA1) pathway in TBI via experimental verifications.

Methods: TBI mouse model induced by weight-drop method was applied in this study. Neurological function tests, Nissl staining, TUNEL staining, and transmission electron microscopy were undertaken to assess the effects of mitophagy on the TBI model. Levels of apoptosis-related factors and mitophagy-related indicators were detected to further reveal the molecular regulatory mechanism of mitophagy in TBI.

Results: Activation of mitophagy (MK-8722 or rapamycin treatment) reduced the severity of brain damage and mitigated neurological function deficits following TBI. MK-8722 treatment reduced neuronal apoptosis, improved neuronal mitophagy, effectively inhibited the expression of proteins Bcl-2 and Bax, and increased the expression of proteins Parkin, PINK1 and OPA1. Besides, MK-8722 improved TBI through accelerating the AMPK/OPA1 pathway, resulting in increase of mitophagy.

Conclusion: This study is the first to pinpoint the AMPK/OPA1 pathway's involvement in TBI and the mechanism of mitophagy, thereby providing a good foundation for future experimental studies.