To analyze the clinical data and imaging examination data of a patient with metallic mercury poisoning from subcutaneous injection. The abdominal B-ultrasonograph results of the patient indicated multiple scattered hyperechoic spots accompanied by "comet tail" sign in the liver and right renal sinus, the nature of which was not clear and it was considered crystal deposition. The chest X-ray revealed scattered and multiple spot-like, snowflake-like and tree-cast-like high-density shadows in both lung fields. The chest computed tomography scan revealed multiple spot and patchy high-density shadows distributed in both lungs, considering hematogenous distribution deposits, and possible mercury poisoning. Laboratory test results showed that blood mercury level was 4.16 μmol/L and urine mercury level was 6 545.5 μg/g Cr. After 28 days of mercury chelation therapy, the abdominal ultrasound examination showed that the hyperechoic spots in the liver and right renal sinus were reduced compared with the previous examination. Metallic mercury poisoning from subcutaneous injection has specific manifestations in abdominal B-ultrasound imaging, which can provide a basis for the early diagnosis of metallic mercury poisoning in clinical practice and can be used to observe the efficacy of mercury chelation therapy.

Due to advances in treatment methods, the survival rate and quality of life of cancer patients have been improved. Radiation-induced vascular injury (RIVI) is a common adverse reaction following radiotherapy, mainly manifested as capillary injury and atherosclerosis in the irradiated area. Radiotherapy induces RIVI in the cerebral vessels, carotid arteries, coronary arteries, and large arteries through mechanisms such as endothelial cell injury and senescence, oxidative stress and inflammatory responses, angiogenesis, and vascular remodeling. In this review research progress in the pathological features, pathophysiological mechanisms, clinical manifestations, prevention and treatment strategies of RIVI was summarized, aiming to provide insights for future research on RIVI.

Radiation-induced rectal injury (RRI) refers to inflammatory intestinal complications of patients with pelvic cavity, abdominal cavity and retroperitoneal tumor during or after radiotherapy, presenting symptoms such as diarrhea, abdominal pain, anal distension, bloody stool, etc. In severe cases, rectovaginal fistula, intestinal obstruction, canceration can occur, adversely affecting the quality of life of patients. The clinical factors of RRI involve total radiotherapy dose, tumor volume, radiotherapy mode and patient-related risk factors. The diagnosis mainly depends on imaging examinations (such as CT, MRI and ultrasound), endoscopy and laboratory examination. The mechanism of RRI is related to intestinal epithelial cell destruction, stem cell injury, microvascular changes and microbial flora imbalance. At present, there is no gold standard for RRI treatment, and the main measures include surgical treatment, internal medicine treatment, hyperbaric oxygen therapy and fecal microbiota transplantation, etc. In this article, the latest progress in the pathogenesis, diagnosis and treatment of RRI was reviewed.

Radiation-induced esophageal injury (RIEI) is a frequent complication following radiotherapy for thoracic and head-neck malignancies, which may lead to severe sequelae including esophageal stricture and perforation, adversely affecting patients' quality of life and therapeutic outcomes. With advancements in radiotherapy techniques — particularly the adoption of unconventional fractionation regimens, concurrent chemoradiotherapy, and combined molecular targeted / immunotherapy — the incidence of RIEI has been increasing. In this review, recent advances in understanding the pathogenesis, clinical manifestations, risk factors, and management strategies for RIEI were comprehensively summarized. Current therapeutic approaches have evolved beyond conventional anti-inflammatory and nutritional support to include novel interventions such as targeted therapy, free radical scavengers, and microbiota modulation, etc. Future research should prioritize the development of optimized, individualized prevention and treatment protocols to mitigate RIEI risk and improve patient prognosis.

The global incidence of head and neck cancer (HNC) is rising, with over 60% of patients presenting at a locally advanced stage. Radiotherapy remains a cornerstone of HNC treatment, and advancements in modern techniques and concurrent chemotherapy have improved local control and survival rates of HNC patients. However, these benefits also bring challenges in the management of toxicities. Due to the proximity of salivary glands and tumors, especially the highly radiosensitive parotid and submandibular glands, this condition is among the most common adverse effects of radiotherapy. Radiation damages acinar cells and ducts, causing glandular atrophy, fibrosis, and reduced saliva secretion, thereby leading to xerostomia and related complications. The risk and severity of injury are associated with the radiation dose and volume affecting the glands. Prevention and management strategies emphasize precise radiotherapy planning, target optimization, and supportive care. Emerging multimodal imaging techniques offer potential for non-invasive prediction and early diagnosis and treatment of radiation-induced salivary gland injury. Future research in regenerative medicine, tissue engineering, and molecular biology aims to elucidate molecular mechanisms, such as signaling pathways and genomics, facilitating personalized strategies to mitigate radiotherapy-induced toxicities and enhance the quality of life of patients.

Osteoradionecrosis of the jaws (ORNJ) is among the most severe oral complications following radiotherapy for head and neck tumors. It is essentially a form of pathological necrosis of the jawbone induced by radiation therapy. ORNJ is defined as bone damage, primarily characterized by inflammation and necrosis, occurring in the jawbone within the irradiated area and accompanied by soft tissue injury, persisting for more than 3 months without spontaneous healing. Diagnosis requires exclusion of other potential etiologies, including primary tumor recurrence, medication-related osteonecrosis, and radiation-induced neoplasms of the jawbone, etc. In this review, recent advances in the epidemiology, risk factors, diagnosis, classification and staging, dosimetric parameters, pathogenesis, treatment, and prevention of radiation-induced osteonecrosis of the jaws were summarized.

Loss-of-function variants of low-density lipoprotein receptor-related protein 5 (LRP5) can lead to reduced bone formation, culminating in diminished bone mass. Our previous study reported transcription factor osterix (SP7)‍-binding sites on the LRP5 promoter and its pivotal role in upregulating LRP5 expression during implant osseointegration. However, the potential role of SP7 in ameliorating LRP5-dependent osteoporosis remained unknown. In this study, we used mice with a conditional knockout (cKO) of LRP5 in mature osteoblasts, which presented decreased osteogenesis. The in vitro experimental results showed that SP7 could promote LRP5 expression, thereby upregulating the osteogenic markers such as alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2), and β‍-catenin (P<0.05). For the in vivo experiment, the SP7 overexpression virus was injected into a bone defect model of LRP5 cKO mice, resulting in increased bone mineral density (BMD) (P<0.001) and volumetric density (bone volume (BV)/total volume (TV)) (P<0.001), and decreased trabecular separation (Tb.‍Sp) (P<0.05). These data suggested that SP7 could ameliorate bone defect healing in LRP5 cKO mice. Our study provides new insights into potential therapeutic opportunities for ameliorating LRP5-dependent osteoporosis.
Animals ; Low Density Lipoprotein Receptor-Related Protein-5/metabolism* ; Osteoporosis/genetics* ; Mice ; Mice, Knockout ; Sp7 Transcription Factor/physiology* ; Osteogenesis ; Bone Density ; Osteoblasts/metabolism* ; Core Binding Factor Alpha 1 Subunit/metabolism* ; Mice, Inbred C57BL ; beta Catenin/metabolism*

Gut microbial communities are likely remodeled in tandem with accumulated physiological decline during aging, yet there is limited understanding of gut microbiome variation in advanced age. Here, we performed a metagenomics-based enterotype analysis in a geographically homogeneous cohort of 367 enrolled Chinese individuals between the ages of 60 and 94 years, with the goal of characterizing the gut microbiome of elderly individuals and identifying factors linked to enterotype variations. In addition to two adult-like enterotypes dominated by Bacteroides (ET-Bacteroides) and Prevotella (ET-Prevotella), we identified a novel enterotype dominated by Escherichia (ET-Escherichia), whose prevalence increased in advanced age. Our data demonstrated that age explained more of the variance in the gut microbiome than previously identified factors such as type 2 diabetes mellitus (T2DM) or diet. We characterized the distinct taxonomic and functional profiles of ET-Escherichia, and found the strongest cohesion and highest robustness of the microbial co-occurrence network in this enterotype, as well as the lowest species diversity. In addition, we carried out a series of correlation analyses and co-abundance network analyses, which showed that several factors were likely linked to the overabundance of Escherichia members, including advanced age, vegetable intake, and fruit intake. Overall, our data revealed an enterotype variation characterized by Escherichia enrichment in the elderly population. Considering the different age distribution of each enterotype, these findings provide new insights into the changes that occur in the gut microbiome with age and highlight the importance of microbiome-based stratification of elderly individuals.
Aged ; Aged, 80 and over ; Female ; Humans ; Male ; Middle Aged ; Bacteroides ; China ; Diabetes Mellitus, Type 2/microbiology* ; Escherichia coli/classification* ; Gastrointestinal Microbiome/genetics* ; Metagenomics ; East Asian People

Due to advances in treatment methods, the survival rate and quality of life of cancer patients have been improved. Radiation-induced vascular injury (RIVI) is a common adverse reaction following radiotherapy, mainly manifested as capillary injury and atherosclerosis in the irradiated area. Radiotherapy induces RIVI in the cerebral vessels, carotid arteries, coronary arteries, and large arteries through mechanisms such as endothelial cell injury and senescence, oxidative stress and inflammatory responses, angiogenesis, and vascular remodeling. In this review research progress in the pathological features, pathophysiological mechanisms, clinical manifestations, prevention and treatment strategies of RIVI was summarized, aiming to provide insights for future research on RIVI.

Radiation-induced rectal injury (RRI) refers to inflammatory intestinal complications of patients with pelvic cavity, abdominal cavity and retroperitoneal tumor during or after radiotherapy, presenting symptoms such as diarrhea, abdominal pain, anal distension, bloody stool, etc. In severe cases, rectovaginal fistula, intestinal obstruction, canceration can occur, adversely affecting the quality of life of patients. The clinical factors of RRI involve total radiotherapy dose, tumor volume, radiotherapy mode and patient-related risk factors. The diagnosis mainly depends on imaging examinations (such as CT, MRI and ultrasound), endoscopy and laboratory examination. The mechanism of RRI is related to intestinal epithelial cell destruction, stem cell injury, microvascular changes and microbial flora imbalance. At present, there is no gold standard for RRI treatment, and the main measures include surgical treatment, internal medicine treatment, hyperbaric oxygen therapy and fecal microbiota transplantation, etc. In this article, the latest progress in the pathogenesis, diagnosis and treatment of RRI was reviewed.