Marrow Injury Research Articles

Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model.

The murine bone marrow injury model is a useful tool to study postnatal osteogenesis through intramembranous ossification. This simplified surgical protocol describes the bone marrow ablation procedure for downstream assessment of new bone formation and cellular responses following injury.

Periosteal skeletal stem cells can migrate into the bone marrow and support hematopoiesis after injury.

Skeletal stem cells have been isolated from various tissues, including periosteum and bone marrow, where they exhibit key functions in bone biology and hematopoiesis, respectively. The role of periosteal skeletal stem cells in bone regeneration and healing has been extensively studied, but their ability to contribute to the bone marrow stroma is still under debate. In the present study, we characterized a whole bone transplantation model that mimics the initial bone marrow necrosis and fatty infiltration seen after injury. Using this model and a lineage tracing approach, we observed the migration of periosteal skeletal stem cells into the bone marrow after transplantation. Once in the bone marrow, periosteal skeletal stem cells are phenotypically and functionally reprogrammed into bone marrow mesenchymal stem cells that express high levels of hematopoietic stem cell niche factors such as Cxcl12 and Kitl. In addition, using in-vitro and in-vivo approaches, we found that periosteal skeletal stem cells are more resistant to acute stress than bone marrow mesenchymal stem cells. These results highlight the plasticity of periosteal skeletal stem cells and their potential role in bone marrow regeneration after bone marrow injury.

Taurine and protocatechuic acid attenuate Vincristine sulphate-induced bone marrow, liver and intestinal injuries via anti-oxidative, anti-inflammatory and anti-apoptotic activities

Taurine and protocatechuic acid attenuate Vincristine sulphate-induced bone marrow, liver and intestinal injuries via anti-oxidative, anti-inflammatory and anti-apoptotic activities

Unraveling the Role of RNase L Knockout in Alleviating Immune Response Activation in Mice Bone Marrow after Irradiation.

Ionizing radiation (IR) induces severe hematopoietic injury by causing DNA and RNA damage as well as activating the immune responses, necessitating the development of effective therapeutic strategies. Ribonuclease L (RNase L) as an innate immune response pathway is triggered by exogenous and endogenous abnormal dsRNA under viral infection and dyshomeostasis, thereby activating the immune responses. Thus, we investigated the effect of RNase L on irradiation-induced bone marrow damage using RNase L knockout (RNase L-/-) mice. Phenotypic analysis revealed that RNase L knockout mitigates irradiation-induced injury in the bone marrow. Further investigation into the mechanism of RNase L by RNA-seq, qRT-PCR, and CBA analysis demonstrated that RNase L deficiency counteracts the upregulation of genes related to immune responses induced by irradiation, including cytokines and interferon-stimulated genes. Moreover, RNase L deficiency inhibits the increased levels of immunoglobulins in serum induced by irradiation. These findings indicate that RNase L plays a role in the immune response induced by irradiation in the bone marrow. This study further enhances our understanding of the biological functions of RNase L in the immune response induced by irradiation and offers a novel approach for managing irradiation-induced bone marrow injury through the regulation of RNase L activation.

Macrophage differentiation in enhancing hematopoietic function of ribonucleic acid for injection II via multi-omics analysis

Ribonucleic acid for injection II is a clinical adjuvant cancer therapy treatment based on immunotherapy, which exerts its effects by enhancing immune function and suppressing tumor growth. However, the mechanism underlying the ameliorative effect on immunosuppressed hematopoietic dysfunction remains unclear. This study confirmed the immune-boosting and hematopoietic-promoting effects of ribonucleic acid for injection II, which has a wide distribution of molecular weights and is rich in amino acids and nucleotides. Ribonucleic acid for injection II influences the gut microbiota and serum metabolites to enhance immunity in immunosuppressed mice induced by CTX, while also mitigating bone marrow injury and increasing hematopoietic cells through mediating macrophage M1 differentiation, thereby improving hematopoietic dysfunction in mice.

Radiomics Texture Analysis of Bone Marrow Alterations in MRI Knee Examinations.

Accurate diagnosis and timely intervention are key to addressing common knee conditions effectively. In this work, we aim to identify textural changes in knee lesions based on bone marrow edema (BME), injury (INJ), and osteoarthritis (OST). One hundred and twenty-one MRI knee examinations were selected. Cases were divided into three groups based on radiological findings: forty-one in the BME, thirty-seven in the INJ, and forty-three in the OST groups. From each ROI, eighty-one radiomic descriptors were calculated, encoding texture information. The results suggested differences in the texture characteristics of regions of interest (ROIs) extracted from PD-FSE and STIR sequences. We observed that the ROIs associated with BME exhibited greater local contrast and a wider range of structural diversity compared to the ROIs corresponding to OST. When it comes to STIR sequences, the ROIs related to BME showed higher uniformity in terms of both signal intensity and the variability of local structures compared to the INJ ROIs. A combined radiomic descriptor managed to achieve a high separation ability, with AUC of 0.93 ± 0.02 in the test set. Radiomics analysis may provide a non-invasive and quantitative means to assess the spatial distribution and heterogeneity of bone marrow edema, aiding in its early detection and characterization.

The effect of platelet infusion on the repair of bone marrow hematopoietic niche damage in mice induced by (60)Co radiation and hematopoietic reconstruction after bone marrow transplantation

Objective: To observe the effect of platelets on hematopoietic stem cell (HSCs) implantation in mice with radiation-induced bone marrow injury and bone marrow transplantation models. Methods: ①Male C57BL/6 mice were divided into a single irradiation group and a radiation infusion group after receiving (60)Co semimyeloablative irradiation for 18-10 weeks. The irradiation infusion group received 1×10(8) platelets expressing GFP fluorescent protein. ② The allogeneic bone marrow transplantation model was established. The experimental groups included the simple transplantation group (BMT) and the transplantation infusion group (BMT+PLT). The BMT group was infused through the tail vein only 5 × 10(6) bone marrow cells, the BMT+PLT group needs to be infused with bone marrow cells at the same time 1× 10(8) platelets. ③ Test indicators included peripheral blood cell and bone marrow cell counts, flow cytometry to detect the proportion of hematopoietic stem cell (HSC) and hematopoietic progenitor cells, bone marrow cell proliferation and apoptosis, and pathological observation of vascular niche damage and repair. Results: ①On the 3rd, 7th, 14(th), and 21st days after irradiation, the bone marrow cell count of the infusion group was higher than that in the single irradiation group (P<0.05), and the peripheral blood cell count was also higher. A statistically significant difference was found between the white blood cell count on the 21st day and the platelet count on the 7th day (P<0.05). In the observation cycle, the percentage of bone marrow cell proliferation in the infusion group was higher, while the percentage of apoptosis was lower. ② The results of bone tissue immunofluorescence after irradiation showed that the continuity of hematopoietic niche with red fluorescence was better in the irradiation infusion group. ③The chimerism percentage in the BMT+PLT group was always higher than that in the BMT group after transplantation.④ The BMT+PLT group had higher bone marrow cell count and percentage of bone marrow cell proliferation on the 7th and 28th day after transplantation than that in the BMT group, and the percentage of bone marrow cell apoptosis on the 14th day was lower than that in the BMT group (P<0.05). After the 14th day, the percentage of stem progenitor cells in the bone marrow cells of mice was higher than that in the BMT group (P<0.05). ⑤The immunohistochemical results of bone marrow tissue showed that the continuity of vascular endothelium in the BMT+PLT group was better than that in the BMT group. Conclusion: Platelet transfusion can alleviate the injury of vascular niche, promotes HSC homing, and is beneficial to hematopoietic reconstruction.

Cytosolic Release of Mitochondrial DNA and Associated cGAS Signaling Mediates Radiation-Induced Hematopoietic Injury of Mice.

Mitochondrion is an important organelle of eukaryotic cells and a critical target of ionizing radiation (IR) outside the nucleus. The biological significance and mechanism of the non-target effect originating from mitochondria have received much attention in the field of radiation biology and protection. In this study, we investigated the effect, role, and radioprotective significance of cytosolic mitochondrial DNA (mtDNA) and its associated cGAS signaling on hematopoietic injury induced by IR in vitro culture cells and in vivo total body irradiated mice in this study. The results demonstrated that γ-ray exposure increases the release of mtDNA into the cytosol to activate cGAS signaling pathway, and the voltage-dependent anion channel (VDAC) may contribute to IR-induced mtDNA release. VDAC1 inhibitor DIDS and cGAS synthetase inhibitor can alleviate bone marrow injury and ameliorate hematopoietic suppression induced by IR via protecting hematopoietic stem cells and adjusting subtype distribution of bone marrow cells, such as attenuating the increase of the F4/80+ macrophage proportion in bone marrow cells. The present study provides a new mechanistic explanation for the radiation non-target effect and an alternative technical strategy for the prevention and treatment of hematopoietic acute radiation syndrome.

Antibacterial and Anti-Biofilm Properties of Diopside Powder Loaded with Lysostaphin

Diopside-based ceramic is a perspective biocompatible material with numerous potential applications in the field of bone prosthetics. Implantable devices and materials are often prone to colonization and biofilm formation by pathogens such as Staphylococcus aureus, which in the case of bone grafting leads to osteomyelitis, an infectious bone and bone marrow injury. To lower the risk of bacterial colonization, implanted materials can be impregnated with antimicrobials. In this work, we loaded the antibacterial enzyme lysostaphin on diopside powder and studied the antibacterial and antibiofilm properties of such material to probe the utility of this approach for diopside-based prosthetic materials. Diopside powder was synthesized by the solid-state method, lysostaphin was loaded on diopside by adsorption, the release of lysostaphin from diopside was monitored by ELISA, and antibacterial and anti-biofilm activity was assessed by standard microbiological procedures. Lysostaphin released from diopside powder showed high antibacterial activity against planktonic bacteria and effectively destroyed 24-h staphylococcal biofilms. Diopside-based materials possess a potential for the development of antibacterial bone grafting materials.

Effect of spermidine on radiation-induced long-term bone marrow cell injury.

Spermidine, a natural polyamine, possesses anti-oxidant, autophagy-regulation, and anti-aging properties. Elevated levels of oxidative stress, which was mediated the senescence of hematopoietic stem cells (HSCs) induced by radiation exposure, may further contribute to long-term myelosuppression. Therefore, this study investigated the protective effect of spermidine on the long-term damage of the hematopoietic system caused by radiation exposure. In vitro experiments, bone marrow mononuclear cells (BMMNCs) of C57BL/6 mice were isolated and incubated with 5mM spermidine for 30min, then irradiated by 2Gy X ray. The survival rate, proliferation, and differentiation ability of BMMNCs were detected. In vivo experiment, mice received 4Gy total body irradiation (TBI), 3mM spermidine were administered in the drinking water every day for 14days prior to irradiation and then continued for 30days after irradiation. Peripheral blood, bone marrow cell typing, level of reactive oxygen species (ROS), colony-forming ability of HSC, and transplantation-reconstitution capability were detected. In vitro experiments, spermidine significantly improved the survival rate of BMMNCs as well as the proliferation and differentiation ability of HSCs exposure to ionizing radiation (IR). In vivo, spermidine reduced levels of ROS in HSCs; spermidine attenuated long-term myeloid differentiation deviation induced by TBI. Spermidine promoted the proliferation and differentiation ability of stem cells, but failed to ameliorate the decreased engraftment capacity of bone marrow cells in mice exposed to TBI. This study demonstrated that spermidine could promote the recovery of IR-induced inhibition of proliferation and differentiation ability of HSCs, partly through antioxidant effects. Whether combining spermidine with other radioprotectants could further increase protective efficacy and reduce the long-term bone marrow injury needs further investigation.

Periosteal Skeletal Stem Cells Can Migrate into the Bone Marrow and Support Hematopoietic Regeneration

Hematopoietic stem cells (HSC) reside within the bone marrow microenvironment, coined the HSC niche, and are supported by various cell types, including bone marrow mesenchymal stem cells (BM-MSCs). BM-MSCs are multipotent stromal cells capable of self-renewal and trilineage differentiation into chondrocytes, osteoblasts, and adipocytes. BM-MSCs secrete factors important for hematopoiesis, such as C-X-C motif ligand 12 (CXCL12) and stem cell factor (SCF). Functional stromal cells are important for bone marrow regeneration after chemotherapy or radiation-induced injury to avoid myelosuppression, a common side effect of these treatments. However, it is not known what governs bone marrow regeneration and how the cells within the bone marrow are repopulated post-injury. Here we describe a novel model of whole bone transplantation to study hematopoietic regeneration and identify periosteal skeletal stem cells (P-SSCs) as key contributors to stromal recovery following bone marrow injury. Skeletal stem cells are skeletal lineage cells that can be found in multiple locations within the body, including the periosteum. The periosteum is a thin, two-layered membrane that covers the surface of bones and has been well studied in the context of bone fracture. P-SSCs can be found in the inner layer of the periosteum and contribute to bone development, regeneration and homeostasis. However, despite the close relationship between bone and bone marrow physiology, the potential role of P-SSCs in hematopoiesis and within the bone marrow has yet to be explored. In this study, we have developed a bone transplantation model that involves isolating a femur from a donor mouse and subcutaneously transplanting it into a recipient mouse (Figure 1A). This model mimics the initial bone marrow cellular necrosis and fatty infiltration seen after bone marrow injury and the subsequent regeneration over time. We discovered that over 99% of the BM-MSCs (CD45-Ter119-CD31-CD51+CD200+) within the engrafted femur were derived from the graft, while over 98% of the hematopoietic cells (CD45+Ter119+) within the engrafted femur were derived from the hosts. Notably, however, we observed that P-SSCs were migrating from the periosteum and into the bone marrow, aiding in stromal regeneration. To assess the contribution of P-SSCs to the recovering bone marrow stroma, we crossed Periostin (Postn)-CreER mice with a tdTomato (Tmt) line. After 5 months, at which point there is no significant difference between host femur and graft femur cellularity, we observed that 83.9% (± 7.18%) of the BM-MSCs within the engrafted femur were Tmt+, indicating periosteal origin (Figure 1B). Once in the bone marrow, these P-SSCs are reprogrammed into BM-MSC-like cells and facilitate hematopoietic recovery, as shown by expression levels of HSC maintenance factors. Compared to steady state P-SSCs, Tmt+ graft BM-MSCs increased CXCL12 and SCF expression by 6.92-fold (p<0.0001) and 5.74-fold (p<0.0001), respectively. Additionally, unlike BM-MSCs, P-SSCs are resistant to transplantation stress, and actively proliferate in the early days following bone transplantation. Using RNA sequencing, qPCR, and flow cytometric analyses, we were able to show that at steady state, P-SSCs appear to be even more quiescent than BM-MSCs, potentially contributing to their stress resistance. Our bone transplantation model has enabled us to study the bone marrow regeneration process using genetic mouse models and led us to uncover a role for P-SSCs in supporting hematopoiesis. Additionally, we have assessed the differential stress response of P-SSCs and BM-MSCs after transplantation. This study highlights a novel bone transplantation model to investigate bone marrow injury and regeneration. It also reveals a critical role of P-SSCs in stromal regeneration and hematopoietic recovery. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Thrombocytopenia in solid malignancies: A review

Thrombocytopenia is one of the most frequent complications associated with cancer or its treatment. Since Radiotherapy and chemotherapy are commonly used for treatment of cancer, Unfortunately, these treatments frequently cause acute and/or long-term bone marrow injury that can adversely affect the quality of life and the course of treatment. There is a need to maintain a safe platelet count to allow effective treatment of the underlying malignancy, prevent bleeding complications and to minimize the use of platelet product transfusion.

Molecular Mechanism of Ferroptosis in Orthopedic Diseases.

Ferroptosis is a new iron-dependent programmed cell death process that is directly mediated by the accumulation of lipid peroxides and reactive oxygen species. Numerous studies have shown that ferroptosis is important in regulating the occurrence and development of bone-related diseases, but the underlying mechanisms are not completely clear. Herein, we review the progress of the mechanism of ferroptosis in bone marrow injury, osteoporosis, osteoarthritis, and osteosarcoma and attempt to deeply understand the regulatory targets of ferroptosis, which will open up a new way for the prevention and treatment of orthopedic diseases.

Haptoglobin is an early indicator of survival after radiation-induced severe injury and bone marrow transplantation in mice

BackgroundHematopoietic stem cell transplantation (HSCT) is the main treatment for acute radiation sickness, especially after fatal radiation. The determination of HSCT for radiation patients is mainly based on radiation dose, hemogram and bone marrow injury severity. This study aims to explore a better biomarker of acute radiation injury from the perspective of systemic immune response.MethodsC57BL/6J female mice were exposed to total body irradiation (TBI) and partial body irradiation (PBI). Changes in haptoglobin (Hp) level in plasma were shown at different doses and time points after the exposure and treatment with amifostine or bone marrow transplantation. Student’s t-test/two tailed test were used in two groups. To decide the Hp levels as a predictor of the radiation dose in TBI and PBI, multiple linear regression analysis were performed. The ability of biomarkers to identify two groups of different samples was determined by the receiver operating characteristic (ROC) curve. The results were expressed as mean ± standard deviation (SD). Significance was set at P value < 0.05, and P value < 0.01 was set as highly significant. Survival distribution was determined by log-rank test.ResultsIn this study, we found that Hp was elevated dose-dependently in plasma in the early post-irradiation period and decreased on the second day, which can be used as a molecular indicator for early dose assessment. Moreover, we detected the second increase of Hp on the 3rd and 5th days after the lethal irradiation at 10 Gy, which was eliminated by amifostine, a radiation protection drug, while protected mice from death. Most importantly, bone marrow transplantation (BMT) on the 3rd and 5th day after 10 Gy radiation improved the 30-days survival rate, and effectively accelerated the regression of secondary increased Hp level.ConclusionsOur study suggests that Hp can be used not only as an early molecule marker of radiation injury, but also as an important indicator of bone marrow transplantation therapy for radiation injury, bringing new scientific discoveries in the diagnosis and treatment of acute radiation injury from the perspective of systemic immunity.

Histopathological Evaluation of Protective Effect of Telmisartan against Radiation-Induced Bone Marrow Injury.

Background: Radiation-induced hematopoietic suppression and myelotoxicity can occur due to the nuclear accidents, occupational irradiation and therapeutic interventions. Bone marrow dysfunction has always been one of the most important causes of morbidity and mortality after ionizing irradiation.Objective: This study aims to investigate the protective effect of telmisartan against radiation-induced bone marrow injuries in a Balb/c mouse model.Material and Methods: In this experimental study, male Balb/c mice were divided into four groups as follow: group 1: mice received phosphate buffered saline (PBS) without irradiation, group 2: mice received a solution of telmisartan in PBS without irradiation, group 3: mice received PBS with irradiation, and group 4: mice received a solution of telmisartan in PBS with irradiation. A solution of telmisartan was prepared and administered orally at 12 mg/kg body weight for seven consecutive days prior to whole body exposing to a single sub-lethal dose of 5 Gy X-rays. Protection of bone marrow against radiation induced damage was investigated by Hematoxylin-Eosin (HE) staining assay at 3, 9, 15 and 30 days after irradiation.Results: Histopathological analysis indicated that administration of telmisartan reduced X-radiation-induced damage and improved bone marrow histology. The number of different cell types in bone marrow, including polymorphonuclear /mononuclear cells and megakaryocytes significantly increased in telmisartan treated group compared to the only irradiated group at all-time points.Conclusion: The results of the present study demonstrated an efficient radioprotective effect of telmisartan in mouse bone marrow against sub-lethal X-irradiation.

Đặc điểm mô bệnh học bệnh lý hoại tử vô khuẩn chỏm xương đùi được phẫu thuật thay khớp háng

Aseptic necrosis of the femoral head (ANFH) accounts for about 2.24% of common joint diseases. The pathophysiological mechanism of ANFH is a lack of blood supply to the femoral head, leading to the death of bone cells and marrow, leading to the collapse and deformation of the femoral head. Objectives: To characterize microscopic damage to femoral head crest in non-traumatic ANFH.Subjects and methods: The study design was a cross-sectional, descriptive study of 31 femoral heads on 31 patients with ANFH who underwent hip replacement surgery at Viet Duc University. The samples were analyzed, processed, and fixed using the HE-stained histological method. Results: All samples had bone marrow damage, of which bone marrow infarction accounted for 58.1%; granulomatous lesions accounted for 71%, fat necrosis and hematopoietic cells accounted for 80.6%; dead bone accounted for 93.3% and new bone formation on dead bone area accounted for 61.3%. Conclusion: Infarct bone marrow injury, fat necrosis, and hematopoietic cells are associated with the formation of granulomatous tissue surrounding the necrotic area. The loss of bone cells in the trabecular is associated with the formation of dead bone fragments. With age, the formation of new bone on the basis of dead bone decreases. * Keywords: Aseptic necrosis; Femoral head; Histopathology.

Clinical Characteristics and Prognosis of Patients with Hematological Malignancies Superimposed with Solid Tumors

To investigate the clinical characteristics and prognosis of hematological malignancies superimposed patients with solid tumors. The clinical data of 30 patients with more than two kinds of malignancy (the second is hematological malignancy) from October 2011 to October 2020 in Department of Hematology, Jiangning Hospital Affiliated to Nanjing Medical University were collected and analyzed retrospectively. The overall survival time was used as the prognostic evaluation standard, and the survival of patients were analyzed by KaplanMeier method. Logrank test and Cox regression model were used to carry out univariate and multivariate retrospective analysis on clinical and laboratory parameters of 30 patients. Among 30 cases, 20 were male, 10 were female, the median age of onset of the second tumor was 70 years old. The common types of the secondary hematological malignancies to solid tumors are myelodysplastic syndrome, acute myeloid leukemia, multiple myeloma. Univariate analysis showed that patients' gender, age, type of solid tumors, the onset of interval between two kinds of tumor, chromosome karyotype were not related to do with the patients' overall survival time. Type of hematologic disease, ECOG score were associated with patients' overall survival time, and the multivariate analysis showed that the type of hematologic disease and ECOG score were independent risk factors for patients with poor prognosis. Patients superimposed with solid tumors complicated with myelodysplastic syndrome or acute leukemia and ECOG score ≥3 have poor prognosis and shorter overall survival time, which are independent risk factors influencing the prognosis. Bone marrow injury, immune dysfunction and genetic susceptibility after chemoradiotherapy may be the main causes of these diseases.

Odontogenic Differentiation-Induced Tooth Regeneration by Psoralea corylifolia L.

Psoralea corylifolia L. (P. corylifolia) has been used as an oriental phytomedicine to treat coldness of hands and feet in bone marrow injury. Hydroxyapatite is usually used for tooth regeneration. In this study, the role of P. corylifolia and bakuchiol, a compound originated from P. corylifolia as differentiation-inducing substances for tooth regeneration, was determined by monitoring odontogenic differentiation in human dental pulp stem cells (hDPSCs). We confirmed that P. corylifolia extracts and bakuchiol increased the odontogenic differentiation of hDPSCs. In addition, the expression of the odontogenic differentiation marker genes alkaline phosphatase (APL), Runt-related transcription factor 2 (RUNX-2), osteocalcin (OC), and dentin matrix acidic phosphoprotein-1 (DMP-1) was proved by real-time polymerase chain reaction, and protein expression of dentin matrix acidic phosphoprotein-1 (DMP-1) and dentin sialophosphoprotein (DSPP) was proved by western blotting. Further, by confirming the increase in small mothers against decapentaplegia (SMAD) 1/5/8 phosphorylation, the SMAD signaling pathway was found to increase the differentiation of odontoblasts. This study confirmed that P. corylifolia L. extracts and bakuchiol alone promote odontogenic differentiation in hDPSCs. These results suggest that bakuchiol from P. corylifolia is responsible for odontogenic differentiation, and they encourage future in vivo studies on dentin regeneration.

Magnetic resonance imaging quantitative analysis of knee joint injury and cartilage before and after long-distance march and training for college students

Objective: To assess the effects of long-distance march and training on acute knee injury and knee cartilage sub-regions of college students using quantitatively magnetic resonance imaging analysis. Methods: Twenty-seven young male students from freshman classes in the Army Military Medical University were enrolled in September 2019, aged from 17 to 20 (19.48±0.14) years, participated in the whole 8-day, 240 km long-distance march and training. Three-dimensional quantitative MRI was performed on the right knee using high-field MRI before (baseline) and 1 day after (follow-up) march. The assessment indexes included: meniscus and cartilage injury(5-point scale), bone marrow and ligament injury, and joint effusion(3-point scale). Using semi-automatic cartilage segmentation and 3D data post-processing techniques, a total of 21 sub-regions of cartilage volume and thickness were measured in the medial and lateral femur, medial and lateral tibia. Paired-samples t-test was used to compare the changes in quantitative cartilage indices of the knee joint before and after march. Results: In terms of acute knee injuries, medial and lateral meniscus injuries (grade 1-3) occurred in 8 and 9 college students, respectively compared with those before march. Anterior cruciate ligaments injury occurred in 4 college students and developed from grade 0 to grade 1. Bone marrow edema occurred in 10 students and developed from grade 0 to grade 2, and in 5 students from grade 0 to grade 1. Joint effusion occurred in 5 college students and developed from grade 1 to grade 2 (all P<0.05). In terms of quantitative analysis of cartilage subregion of knee joint, the volume of central region of femoral pulley increased [(1.84±0.32) mm3 vs (1.67±0.29) mm3] and the volume of central region of medial femoral condyle decreased [(1.18±0.21) mm3 vs (1.26±0.17) mm3] compared with that before march (all P<0.05); The cartilage thickness of 11 cartilage subregion [(1.37±0.27) mm vs (1.53±0.18) mm], [(1.42±0.25) mm vs (1.54±0.17) mm], [(1.53±0.20) mm vs (1.62±0.20) mm], [(1.72±0.28) mm vs (1.83±0.28) mm], [(1.84±0.45) mm vs (2.04±0.42) mm], [(2.20±0.58) mm vs (2.46±0.50) mm], [(1.74±0.19) mm vs (1.85±0.21) mm] [(1.45±0.21) mm vs (1.58±0.16) mm], [(1.81±0.22) mm vs (1.91±0.15) mm], [(1.44±0.13) mm vs (1.53±0.15) mm] was thinner than that before march (all P<0.05). The T2 values of 7 cartilage subregion [(40.57±26.23) ms vs (67.10±47.46) ms], [(80.10±20.56) ms vs (98.42±23.58) ms], [(87.92±24.95) ms vs (108.84±29.24) ms], [(50.49±19.18) ms vs (76.97±37.16) ms], [(38.89±15.82) ms vs (69.70±40.16) ms] [(55.84±24.53) ms vs (106.35±50.01) ms] and [(72.38±36.64) ms vs (105.31±39.34) ms] were lower than those before march, while the T2 values of the two subregions of patellar cartilage [(102.13±44.47) ms vs (72.20±28.37) ms], [(97.42±44.86) ms vs (76.67±51.64) ms] were higher than those before march (P<0.05). There was no significant difference in other cartilage subareas (P>0.05). Conclusions: Long distance hiking will lead to acute injury of knee joint of young college students. The thickness of cartilage subregion of knee joint showed a thinning trend as a whole, while the volume and T2 values showed different trends.

Aspirin Protective Effect on Cyclophosphamide Induced Hematological Toxicity

Bone marrow toxicity is the most important factor limiting the use of cytotoxic drugs like alkylating agents in cancer treatment. Recently PG synthase enzyme inhibitors have been reported to potentiate the cytotoxic effects of these agents on cancer cells but little is known if they can affect the toxicity of these agents on bone marrow or other tissues. Cyclophosphamide is one of the most commonly used alkylating agent. In the present work, the effect of these PG synthase enzyme inhibitors, aspirin on cyclophosphamide myelotoxicity was determined employing the peripheral blood count to reflect bone marrow injury. The effect on body weight changes caused by cyclophosphamide was also determined. Cyclophosphamide in doses of 25, 50 and 75 mg/kg i. v. produced as a dose dependent reduction in total WBC count, granulocyte, non granulocyte, and Hb% which was maximum on second day after injection and still present on 5th day post injection. It also produced a dose dependent reduction in body weight on day 5 after injection. Aspirin in doges of 75, 150 and 300 mg/kg i. m. protected against the reduction in WBC counts 'measured for 5 days after injection of cyclophosphamide (50 mg/kg). This protection was not dose dependent, though it was more optimum with 300 mg/kg and disappeared largely when a dose of 450 mg/kg was used. Aspirin did not prevent the changes in Hb% but retard the reduction in body weight caused by cyclophosphamide. It is concluded that aspirin can help to reduce injury and enhance recovery from bone marrow toxicity caused by cytotoxic agents such as the alkylating drugs cyclophosphamide for which no specific antidote is available. Aspirin produces this effect possibly by eliminating the harmful inhibitory effect of excess PGs or leukotrienes, released by bone marrow injury on growth factors of haemopoietic progenitor cells. The magnitude of this protection on WBC counts does not seem to differ between either PG synthase enzyme inhibitors or steroids when used alone or in combination although a synergistic effect in protecting erythropoiesis is observed.