Low Back Pain in Resident Doctors with Standardized Training in China: A Cross-Sectional Study.

Background: Low back pain (LBP) is a prevalent occupational disease with high morbidity among healthcare workers. Since the implementation of standardized residency training in China in 2015, the training intensity has significantly increased, which may lead to a higher incidence of LBP. However, epidemiological studies on LBP among resident doctors with standardized training remain scarce. Objective: To investigate the prevalence and associated factors of LBP among resident doctors with standardized training in a tertiary hospital in China. Methods: A cross-sectional study was conducted using self-administered questionnaires to collect information on demographics, lifestyle factors, work-related factors, and LBP from 345 resident doctors. Descriptive statistics were used to analyze the prevalence of LBP. Logistic regression analysis was performed to identify factors associated with LBP. Results: Among 345 participants, the 1-year prevalence of LBP was 75.9%. Multivariable analysis revealed that physical exercise, weekly working hours, and prolonged sitting were independent risk factors for LBP. Conclusion: The prevalence of LBP among resident doctors was high. Promoting physical exercise, controlling working hours, and improving sitting posture may help prevent LBP. The study was limited by its cross-sectional design and self-reported data. Future studies should use longitudinal designs, objective measures, and larger and more representative samples to further explore the epidemiology and etiology of LBP among resident doctors with standardized training.

The Association Between Blood Pressure and Headache in Postmenopausal Women: A Prospective Hospital-Based Study.

BACKGROUND: Headache is the most frequent condition for outpatient patients because of neurological problems, but little is known about predisposing and enabling factors for headache patients. AIM: To investigate the association between blood pressure (BP) and headache in postmenopausal women. METHODS: The postmenopausal women who were admitted to our hospital from January 2015 to December 2019 were screening according to the criteria. Their systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP) were assessed and the information of age, body mass index, smoking status, caffeine consumption, cholesterol levels, and daily alcohol use were collected. Multiple logistic regression model was established to evaluate the association between BP and headache. RESULTS: A total of 1571 postmenopausal women were included in the analysis, including 953 headache-free population and 618 headache participants during the studied periods. We found that increasing SBP and PP were associated with the lower occurrence of migraine, tension-type headache (TTH), probable migraine, and unclassified headache (P < 0.05). However, there was a negative association between DBP levels and the new occurrence of overall headache, but we did not find any relations of DBP with any subtypes of headache. CONCLUSION: There were negative associations of SBP and PP with new occurrence of headache, especially migraine and TTH, but there is no relationship between DBP and the subsequent development of headache.

Polydatin prevents the induction of secondary brain injury after traumatic brain injury by protecting neuronal mitochondria.

Polydatin is thought to protect mitochondria in different cell types in various diseases. Mitochondrial dysfunction is a major contributing factor in secondary brain injury resulting from traumatic brain injury. To investigate the protective effect of polydatin after traumatic brain injury, a rat brain injury model of lateral fluid percussion was established to mimic traumatic brain injury insults. Rat models were intraperitoneally injected with polydatin (30 mg/kg) or the SIRT1 activator SRT1720 (20 mg/kg, as a positive control to polydatin). At 6 hours post-traumatic brain injury insults, western blot assay was used to detect the expression of SIRT1, endoplasmic reticulum stress related proteins and p38 phosphorylation in cerebral cortex on the injured side. Flow cytometry was used to analyze neuronal mitochondrial superoxide, mitochondrial membrane potential and mitochondrial permeability transition pore opened. Ultrastructural damage in neuronal mitochondria was measured by transmission electron microscopy. Our results showed that after treatment with polydatin, release of reactive oxygen species in neuronal mitochondria was markedly reduced; swelling of mitochondria was alleviated; mitochondrial membrane potential was maintained; mitochondrial permeability transition pore opened. Also endoplasmic reticulum stress related proteins were inhibited, including the activation of p-PERK, spliced XBP-1 and cleaved ATF6. SIRT1 expression and activity were increased; p38 phosphorylation and cleaved caspase-9/3 activation were inhibited. Neurological scores of treated rats were increased and the mortality was reduced compared with the rats only subjected to traumatic brain injury. These results indicated that polydatin protectrd rats from the consequences of traumatic brain injury and exerted a protective effect on neuronal mitochondria. The mechanisms may be linked to increased SIRT1 expression and activity, which inhibits the p38 phosphorylation-mediated mitochondrial apoptotic pathway. This study was approved by the Animal Care and Use Committee of the Southern Medical University, China (approval number: L2016113) on January 1, 2016.

Inhibition of endoplasmic reticulum stress alleviates secondary injury after traumatic brain injury.

Apoptosis after traumatic brain injury has been shown to be a major factor influencing prognosis and outcome. Endoplasmic reticulum stress may be involved in mitochondrial mediated neuronal apoptosis. Therefore, endoplasmic reticulum stress has become an important mechanism of secondary injury after traumatic brain injury. In this study, a rat model of traumatic brain injury was established by lateral fluid percussion injury. Fluorescence assays were used to measure reactive oxygen species content in the cerebral cortex. Western blot assays were used to determine expression of endoplasmic reticulum stress-related proteins. Hematoxylin-eosin staining was used to detect pathological changes in the cerebral cortex. Transmission electron microscopy was used to measure ultrastructural changes in the endoplasmic reticulum and mitochondria. Our results showed activation of the endoplasmic reticulum stress-related unfolded protein response. Meanwhile, both the endoplasmic reticulum stress response and mitochondrial apoptotic pathway were activated at different stages post-traumatic brain injury. Furthermore, pretreatment with the endoplasmic reticulum stress inhibitor, salubrinal (1 mg/kg), by intraperitoneal injection 30 minutes before injury significantly inhibited the endoplasmic reticulum stress response and reduced apoptosis. Moreover, salubrinal promoted recovery of mitochondrial function and inhibited activation of the mitochondrial apoptotic pathway post-traumatic brain injury. These results suggest that endoplasmic reticulum stress might be a key factor for secondary brain injury post-traumatic brain injury.