Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences最新文献

The canalis sinuosus, a canal containing the anterior superior alveolar nerve bundle, originates from the infraorbital canal and extends along the maxillary sinus and nasal cavity edges to the anterior maxilla. It was once regarded as an anatomical variation. However, with the widespread application of cone beam computed tomography (CBCT), the detection rate of canalis sinuosus in the population has increased. The canalis sinuosus exhibits diverse courses, branching into multiple accessory canals and terminating at the nasal floor or the anterior tooth region, with the majority traversing the palatal side of the central incisor. The anterior superior alveolar nerve bundle within the canalis sinuosus not only innervates and nourishes the maxillary anterior teeth and the corresponding soft tissues, and the maxillary sinus mucosa, but also relates to the nasal septum, lateral nasal wall, and parts of the palatal mucosa. To minimize surgical complications, strategies for preventing and treating canalis sinuosus injuries need to be investigated. Preoperatively, CBCT is used to identify the canalis sinuosus and to virtually design implant placement at a distance of more than 2 mm from the canalis sinuosus. Intraoperatively, assessing bleeding and patient comfort, complemented by precision surgical techniques such as the use of implant surgical guide plates. Postoperatively, CBCT is used to examine the relationship between the implant and the canalis sinuosus, and treatment of canalis sinuosus injuries can be tailored based on the patient's symptoms. This review summarizes the detection of canalis sinuosus in the population, its anatomical characteristics, and the physiological functions in the anterior maxilla, and discusses strategies for avoiding canalis sinuosus injuries during implant surgery, thereby enhancing clinical awareness and providing references for clinical decision-making.

Iron metabolism refers to the process of absorption, transport, excretion and storage of iron in organisms, including the biological activities of iron ions and iron-binding proteins in cells. Clinical research and animal experiments have shown that iron metabolism is associated with the progress of periodontitis. Iron metabolism not only enhances the proliferation and toxicity of periodontal pathogens, but also activate host immune-inflammatory response mediated by macrophages, neutrophils and lymphocytes. In addition, iron metabolism is also involved in regulating cellular death sensitivity of gingival fibroblasts and osteoblasts and promoting the differentiation of osteoclasts, which plays a regulatory role in the regeneration and repair of periodontal tissue. This article reviews the research progress on the pathogenesis of periodontitis from the perspective of iron metabolism, aiming to provide new ideas for the treatment of periodontitis.

Macrophages are vital in maintaining tissue homeostasis in the lungs by modulating and regulating immune responses. Based on different origins and anatomical locations, macrophages in the lungs are categorized into alveolar macrophages, interstitial macrophages, perivascular macrophages, and inflammatory macrophages. Alveolar macrophages are located in the alveolar spaces and are primarily responsible for maintaining alveolar surfactant homeostasis, defending against pathogens and regulating immune responses. Interstitial macrophages can maintain homeostasis, regulate immunity and anti-inflammation in the lung tissue. Perivascular macrophages play a crucial role in inhibiting lung inflammation, improving pulmonary fibrosis, and regulating lung tumor progression due to antigen-presenting and immunomodulatory effects. Inflammatory macrophages, which are differentiated from monocytes during inflammation, regulate the inflammatory process. This article reviews the origins of various subpopulations of macro-phages in the lung tissue and their physiological and pathological functions as well as discusses the underlying mechanisms and potential therapeutic targets.

Objectives: To establish a cell line stably expressing the transient receptor potential melastatin 2 (TRPM2) channel for screening TRPM2 inhibitors based on PiggyBac transposition system.

Methods: A plasmid PiggyBac-human TRPM2 (pPB-hTRPM2) eukaryotic expression vector was constructed using PiggyBac transposition system. The plasmid and a helper plasmid were co-transfected into HEK293T cells to express TRPM2, which was identified by fluorescence and patch-clamp assays. The high throughput screening performance was assessed with the Z ´ factor. Calcium imaging and patch clamp techniques were employed to assess the initial activity of eleven compound molecules, confirming the inhibitory effects of the primary molecules on TRPM2. The protective effect of the screened compounds on damaged cells was validated using the oxygen-glucose deprivation/reperfusion (OGD/R) injury model and CCK-8 kit. The level of cellular reactive oxygen species (ROS) was detected by flow cytometry. The neuroprotective effects of the compounds were evaluated using a transient middle cerebral artery occlusion (tMCAO) mouse model.

Results: The HEK293T cells transfected with pPB-hTRPM2-EGFP showed high TRPM2 expression. Puromycin-resistant cells, selected through screening, exhibited robust fluorescence. Whole-cell patch results revealed that induced cells displayed classical TRPM2 current characteristics comparable to the control group, showing no significant differences (P>0.05). With a Z ´ factor of 0.5416 in calcium imaging, the model demonstrated suitability for high-throughput screening of TRPM2 inhibitors. Calcium imaging and electrophysiological experiments indicated that compound 6 significantly inhibited the TRPM2 channel. Further experiments showed that 1.0 μmol/L of compound 6 enhanced cell viability (P<0.05) and reduced the level of ROS (P<0.05) of SH-SY5Y under OGD/R injury. 0.3 and 1.0 mg/kg of compound 6 reduced the cerebral infarction volume in tMCAO mice (both P<0.05).

Conclusions: A stable TRPM2 gene expressing cell line has been successfully established using PiggyBac gene editing in this study. TRPM2 channel inhibitors were screened through calcium imaging and patch clamp techniques, and an inhibitor compound 6 was identified. This compound can alleviate cell damage after OGD/R by reducing cellular ROS levels and has a protective effect against cerebral ischemia-reperfusion injury in mice.

A 15-year-old female with Hodgkin's lymphoma underwent ovarian tissue cryopreservation for preserving fertility in Reproductive Department of Sir Run Run Shaw Hospital, Zhejiang University School of Medical after receiving one course of chemotherapy. During the ovarian tissue cryopreservation, one MⅡmature oocyte and three germinal vesicle oocytes were found. The three immature oocytes underwent in vitro maturation but failed. Ultimately, one mature oocyte and 12 ovarian cortex slices were cryopreserved using vitrification. This case indicates that for patients with established gonadal axis feedback, ovarian tissue cryopreservation may not be the only method for fertility preservation. It is advisable to consider ovarian stimulation and oocyte retrieval for oocyte cryopreservation. Alternatively, for individuals in the ovulation phase of their menstrual cycle, attempting oocyte retrieval before ovarian tissue cryopreservation to obtain mature oocytes from the natural cycle, followed by oocyte cryopreservation, may enhance the likelihood of successful fertility preservation.

Objectives: To explore the diagnostic value of ultrasonography for injuries of anterior talofibular ligament (ATFL) and anterior inferior tibiofibular ligament distal fascicle (ATiFL-DF) in patients with ankle fractures.

Methods: Clinical data of 51 patients with ankle fractures who were clinically suspected of ligament injuries and underwent ankle ultrasonography examination and arthroscopy in Sir Run Run Shaw Hospital, Zhejiang University School of Medicine from April 2019 to March 2023 were retrospectively analyzed. Using arthroscopic results as the gold standard, the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of ultrasonography in diagnosing ATFL and ATiFL-DF injuries were evaluated, and Kappa consistency test was performed.

Results: The sensitivity and specificity of ultrasonography in diagnosis of ATFL injury were 100.0% and 92.3%, with the PPV of 92.6% and NPV of 100.0%. Ultrasonography findings exhibited excellent concordance with arthroscopic results (kappa=0.849). The sensitivity and specificity of ultrasonography in diagnosis of ATiFL-DF injury was 86.7% and 33.3%, with the PPV of 90.7% and NPV of 25.0%. However, the consistency between ultrasonography and arthroscopic results was poor (kappa=0.168).

Conclusions: Ultrasonography is reliable in assessing injuries of ATFL in patients with ankle fractures, but its specificity in diagnosing ATiFL-DF is poor. Therefore, ankle arthroscopy remains necessary for ankle fracture patients with negative findings of ATiFL-DF in ultrasonography.

Basivertebral foramen is a natural orifice in the posterior wall of the vertebral body existing in humans and mammals, through which the basal vertebral vein, branch of lumbar artery and recurrent branch of spinal nerve enter and exit the vertebral body. Basivertebral foramen changes the local microstructure of the vertebral body, resulting in cortical defect and sparse trabecular bone in the central region of the vertebral body, thus affecting its biomechanical characteristics and making its central region a "weak" area of the vertebra. Some characteristic injuries of the vertebra are related to basivertebral foramen, such as vertebral compression fracture and intervertebral cleft, vertebral burst fracture and posterior upper vertebral fracture fragment, and cement leakage during treatment. In this article, the anatomical and developmental biological characteristics of basivertebral foramen, the impact of basivertebral foramen on biomechanical characteristics, and the treatment of basivertebral foramen related vertebral diseases are reviewed, in order to provide references for the clinical diagnosis and treatment of vertebral injuries.

Objectives: To investigate the effect of sinusoidal alternating electromagnetic field (SEMF) on fracture healing and its mechanism.

Methods: Femoral fracture model was established using specific pathogen free male Wistar rats. Thirty rats were randomly divided into the control and SEMF groups with 15 rats in each group. The SEMF group was given 50 Hz 1.8 mT for 90 min every day, while the control group was not treated. X-ray examinations were performed every two weeks to determine the formation of bone scabs. Three rats from both groups were sacrificed after 2 and 4 weeks of treatment. Protein was extracted from the fractured femurs, and the expression of type Ⅰ collagen (COL-1), osterix (OSX), Runt-related transcription factor 2 (RUNX2), and vascular endothelial growth factor (VEGF) was detected by Western blotting. After 8 weeks, the femur on the operated side was taken for micro-CT scanning to observe fracture healing, angiography to observe blood vessel growth, and organs such as hearts, livers, spleens, lungs, and kidneys were taken for safety evaluation by hematoxylin-eosin staining (HE staining).

Results: The bone scab scores of the SEMF group were significantly higher than those of the control group after 2, 4, 6, and 8 weeks of treatment (all P<0.01). The fracture healing of the SEMF group was better than that of the control group after 8 weeks, and the bone volume scores of the two groups were 0.243±0.012 and 0.186±0.008, respectively (P<0.01); the number of blood vessels in the SEMF group was also more than that of the control group after 8 weeks. Western blotting results showed that the expressions of COL-1, OSX, RUNX2, and VEGF were higher in the SEMF group than those in the control group after 2 and 4 weeks of treatment (all P<0.05). HE staining showed that histopathological results of the examined organs were normal in both groups.

Conclusions: SEMF can accelerate fracture healing by promoting the expression of osteogenic factors and vascular proliferation without significant adverse effects.