Morphological study of superficial palmar arch and the significance in clinical operation.

BACKGROUND: The superficial palmar arch is a crucial blood supply to the palm. However, it exhibits significant variations, posing challenges in surgical procedures. Gaining a comprehensive understanding of the relationship between different types, physiological indices, and the clinical significance of the superficial palmar arch will enhance the accuracy of diagnosing and treating patients. MATERIALS AND METHODS: In this study, we dissected a total of 72 specimens, comprising 39 males and 33 females. We observed the type, length, and diameter of the superficial palmar arch and analyzed its correlation with the disease. Additionally, we conducted Doppler ultrasound measurements on 20 healthy volunteers (10 males and 10 females) and 18 patients with superficial palmar arch injury (10 males and 8 females) to assess the classification, diameter, intimal thickness, and blood flow velocity of the superficial palmar arch. We collected information on 9 male patients with finger fracture and observed the classification of the superficial palmar arch, fracture healing time, and basic function recovery time. Lastly, we analyzed rare variant specimens encountered during the anatomy process. RESULTS: In the exploration of human anatomy, there were four types of superficial palmar arch: ulnar artery arch type in 17 cases (23.61%), radial ulnar artery type in 46 cases (63.89%), ulnar artery without arch type in 6 cases (8.33%), and 3 cases (4.17%) of double arch type of radial and ulnar artery. One case non-arched type was found in imaging examination (5%). In one elderly male specimen, the hand's superficial palmar arch artery was tortuous and dilated. In addition, there was a positive correlation between the diameter and length of the superficial palmar arch (except the second common palmar digital artery in women), among which the ulnar artery and the third common palmar digital artery had the strongest correlation. Compared to healthy volunteers, patients with ulnar injury in the Radial-ulnar artery type exhibited a decrease in the diameter and blood flow velocity of the ulnar artery, as well as the second and third common palmar digital arteries. No such change was observed in patients with radial injury. Additionally, patients with ulnar injury in other types of Radial-ulnar artery also experienced a decrease in the diameter and blood flow velocity of the ulnar artery. Finger fracture patients with Ulnar artery with arch and Ulnar artery without arch had shorter fracture healing time and basic function recovery time compared to those with Radial-ulnar artery type. CONCLUSIONS: This study investigated the relationship between the classification, physiological index, and clinical significance of the superficial palmar arch at all levels. The results demonstrated that when the superficial palmar arch is damaged, it is important to consider both the classification and the site of damage, as this can potentially result in improved therapeutic outcomes. These findings provide a basis for future clinical research.

Fluoride induces osteoblast autophagy by inhibiting the PI3K/AKT/mTOR signaling pathway in vivo and in vitro.

Fluorosis primarily manifests as bone damage in the form of dental fluorosis and skeletal fluorosis and represents a critical global public health challenge. However, few studies have examined autophagy-related signaling pathways in skeletal fluorosis. This study aimed to investigate the effect of fluoride on autophagy in osteoblasts using comprehensive methods and to explore the role of the PI3K/AKT/mTOR signaling pathway in regulating fluoride-induced autophagy in osteoblasts. Sprague-Dawley (SD) rats were exposed to different concentrations of fluoride (NaF: 5, 50, and 100 mg/L) for six months. Primary osteoblasts were treated with 0.5, 1.0, or 3.0 mM NaF. Hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), immunohistochemistry (IHC), immunofluorescence staining, and western blotting were performed to evaluate morphological changes in bone tissues and autophagosomes and to detect the protein expression of autophagy-related markers and PI3K/AKT/mTOR signaling pathway-related molecules both in vivo and in vitro. The bone tissues of fluoride-exposed rats showed osteosclerosis, autophagosomes and autolysosomes. LC3B immunofluorescence staining revealed an increase in autophagosomes in the primary osteoblasts treated with fluoride. The LC3Ⅱ/Ⅰ ratio and levels of autophagy-related markers (Beclin 1 and Atg7) were increased, whereas P62 levels were decreased in bone tissues and primary osteoblasts in the fluoride groups. Simultaneously, p-AKT and p-mTOR levels were reduced in bone tissues and primary osteoblasts in the fluoride groups. Moreover, a PI3K inhibitor (LY294002) further downregulated p-AKT and p-mTOR protein expression but slightly increased the LC3Ⅱ/Ⅰ ratio in primary osteoblasts. These results demonstrate that fluoride induces autophagy in osteoblasts by inhibiting the PI3K/AKT/mTOR signaling pathway, which deepens our understanding of the molecular mechanisms underlying fluoride-induced bone damage and provides a theoretical basis for the prevention and treatment of skeletal fluorosis.

Expression of Autophagy-Related Factors LC3A and Beclin 1 and Apoptosis-Related Factors Bcl-2 and BAX in Osteoblasts Treated With Sodium Fluoride.

OBJECTIVE: This study aims to analyze the expressions of autophagy-related factors light chain 3 alpha (LC3A) and Beclin 1 and apoptosis-related factors B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (BAX) in primary osteoblasts treated with sodium fluoride (NaF). METHODS: Osteoblasts were extracted from Sprague-Dawley rats and treated with 0, 2.5, 5, and 10 mg/L NaF solutions, followed by 10 mmol/L 3-methyladenine (3-MA) for 24 h. The apoptotic rate was determined by flow cytometry, and the expressions of the autophagy- and apoptosis-related factors were measured by western blotting and real-time quantitative polymerase chain reaction. RESULTS: The mRNA expressions of LC3A, Beclin 1, and BAX in the NaF-treated osteoblast group were higher than those in the control group, while the protein expressions of these factors in the NaF-treated group were significantly higher than those in the control group. However, the Bcl-2 protein expression in the NaF-treated osteoblasts was significantly decreased compared to that in the control cells. After the 3-MA treatment, the protein expressions of LC3A, Beclin 1, and Bcl-2 were significantly decreased compared with those of the NaF-treated group, whereas the expression of BAX increased. Moreover, the apoptosis rate was increased after the addition of the 3-MA inhibitor. CONCLUSION: NaF stimulation promoted autophagy and apoptosis of the osteoblasts, suggesting the involvement of fluoride damage in these processes.

The value of the hedgehog signal in osteoblasts in fluoride-induced bone-tissue injury.

OBJECTIVE: This study was designed to observe the expression of important hedgehog (Hh) signal factors in the bone tissue of rats with chronic fluorosis and cultured osteoblasts in order to investigate the role and significance of the Hh signal in fluoride-induced bone injury. METHODS: Healthy Sprague-Dawley (SD) rats were randomly divided into four groups: the control group, the fluorosis group (F Group), the fluoride + blocker group (F + Cycl group: rats were treated with fluoride + cyclopamine), and the fluoride + blocker control group (F + DMSO group). After 6 months of intervention, the urinary fluoride content of rats in each group was detected. The primary osteoblasts of rats were selected for cell experiment, and the experiment was carried out after the cells were passaged from the second to the fourth generation. RESULTS: The proliferation rate of primary rat osteoblasts presented time-affected and dose-affected relationships in a short time under treatment with a low dose of sodium fluoride (NaF), but the proliferation of osteoblasts was inhibited by long-term and high-dose NaF exposure. In the F group, the alkaline phosphatase (ALP) activity of osteoblasts increased gradually. The ALP activity was lower in the F + Cycl group than in the F group, and there was no significant difference between the F + DMSO group and F group. With the increase in fluoride exposure, the expression of Hh signal factors and osteogenic-related factor proteins increased gradually. The expressions of Indian hedgehog (Ihh), smoothened (Smo), Glioma-associated oncogene homolog (Gli) 2, and Runt-related transcription factor 2 (Runx2)in the F + Cycl group increased with the dose of fluoride but they were significantly inhibited compared with the F group. Compared with the control group, the content of urinary fluoride in the F group was significantly higher (P < 0.05), but there was no significant change in urinary fluoride content in the F + Cycl group and the F + DMSO group. Compared with the control group, the serum bone alkaline phosphatase (BALP) contents of rats in the other groups increased after 6 months' intake of fluoride water (P < 0.05). After drug blocking, the serum BALP content in the F + Cycl group was lower than that in the F + DMSO group (P < 0.05). The BALP content in the F + DMSO group was similar to that in the F group: it did not decrease. The mRNA expressions of Ihh, Smo, Gli2, and Runx2 in bone tissue of the F group were significantly higher than those in the control group (P < 0.05). After cyclopamine blocking, the expressions decreased (P < 0.05), but the differences between the F + DMSO group and F group were not statistically significant. CONCLUSION: Hh signal plays an important role in fluoride-induced bone injury. The effective inhibition of cyclopamine is expected to be a new target for the treatment of skeletal damage caused by fluorosis.

Exercise Prevents Memory Impairment Induced by Arsenic Exposure in Mice: Implication of Hippocampal BDNF and CREB.

High concentrations of arsenic, which can be occasionally found in drinking water, have been recognized as a global health problem. Exposure to arsenic can disrupt spatial memory; however, the underlying mechanism remains unclear. In the present study, we tested whether exercise could interfere with the effect of arsenic exposure on the long-term memory (LTM) of object recognition in mice. Arsenic (0, 1, 3, and 10 mg/ kg, i.g.) was administered daily for 12 weeks. We found that arsenic at dosages of 1, 3, and 10 mg/kg decreased body weight and increased the arsenic content in the brain. The object recognition LTM (tested 24 h after training) was disrupted by 3 mg/ kg and 10 mg/ kg, but not 1 mg/ kg arsenic exposure. Swimming exercise also prevented LTM impairment induced by 3 mg/ kg, but not with 10 mg/ kg, of arsenic exposure. The expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP-response element binding protein (pCREB) in the CA1 and dentate gyrus areas (DG) of the dorsal hippocampus were decreased by 3 mg/ kg and 10 mg/ kg, but not by 1 mg/ kg, of arsenic exposure. The decrease in BDNF and pCREB in the CA1 and DG induced by 3 mg/ kg, but not 10 mg/ kg, of arsenic exposure were prevented by swimming exercise. Arsenic exposure did not affect the total CREB expression in the CA1 or DG. Taken together, these results indicated that swimming exercise prevented the impairment of object recognition LTM induced by arsenic exposure, which may be mediated by BDNF and CREB in the dorsal hippocampus.

Observations on pathological and histochemical changes in piglet livers infected with Taenia saginata asiatica.

To study the pathological and histochemical characteristics of lesions in piglet livers infected with Taenia saginata asiatica (T. saginata asiatica) throughout the different stages, piglets were fed with eggs of T. saginata asiatica and raised in isolation in an animal center to establish the T. saginata asiatica infection model with normal piglets as control. The pathological changes in the piglet livers were observed after the infection using liver sections stained with hematoxylin and eosin. Histochemical methods were used to check the changes in lipid, glycogen and protein content in the liver. The data collected by image analysis were analyzed statistically with Statistical Package for the Social Science. The results show that T. saginata asiatica-exposed piglets were indeed infected. Inflammatory reactions began on the fourth day and progressed rapidly. Kupffer cell hyperplasia, hepatic hydropic degeneration and ballooning degeneration were found in the 10th-20th days after infection. Hepatic central veins and hepatic sinusoids were dilated and congested. Spotty necrosis occurred in some local liver tissues. In the 40th-60th days, granulomatous reactions and mild hepatocirrhosis were the main lesions. In the 70th-80th days, hepatocirrhosis and bile duct proliferation were observed in the liver. In the different stages, lipid drops were increased while glycogen and protein levels were decreased to some degree. There was a significant difference in metabolism between the infected group and the control group (P < 0.01). It is concluded that pigs are the favorable intermediate host of T. saginata asiatica and its infection can result in serious pathological and histochemical lesions in host organs.