ABSTRACT
Social pain, a multifaceted emotional response triggered by interpersonal rejection or criticism, profoundly impacts mental well-being and social interactions. While prior research has implicated the right ventrolateral prefrontal cortex (rVLPFC) in mitigating social pain, the precise neural mechanisms and downstream effects on subsequent social attitudes remain elusive. This study employed transcranial magnetic stimulation (TMS) integrated with fMRI recordings during a social pain task to elucidate these aspects. Eighty participants underwent either active TMS targeting the rVLPFC (n = 41) or control stimulation at the vertex (n = 39). Our results revealed that TMS-induced rVLPFC facilitation significantly reduced self-reported social pain, confirming the causal role of the rVLPFC in social pain relief. Functional connectivity analyses demonstrated enhanced interactions between the rVLPFC and the dorsolateral prefrontal cortex, emphasizing the collaborative engagement of prefrontal regions in emotion regulation. Significantly, we observed that negative social feedback led to negative social attitudes, whereas rVLPFC activation countered this detrimental effect, showcasing the potential of the rVLPFC as a protective buffer against adverse social interactions. Moreover, our study uncovered the impact role of the hippocampus in subsequent social attitudes, a relationship particularly pronounced during excitatory TMS over the rVLPFC. These findings offer promising avenues for improving mental health within the intricate dynamics of social interactions. By advancing our comprehension of the neural mechanisms underlying social pain relief, this research introduces novel intervention strategies for individuals grappling with social distress. Empowering individuals to modulate rVLPFC activation may facilitate reshaping social attitudes and successful reintegration into communal life.
Subject(s)
Magnetic Resonance Imaging , Prefrontal Cortex , Transcranial Magnetic Stimulation , Humans , Transcranial Magnetic Stimulation/methods , Male , Female , Young Adult , Prefrontal Cortex/physiology , Prefrontal Cortex/diagnostic imaging , Prefrontal Cortex/physiopathology , Adult , Attitude , Social Interaction , Pain/physiopathology , Pain/psychology , Brain Mapping/methods , Dorsolateral Prefrontal Cortex/physiology , Dorsolateral Prefrontal Cortex/diagnostic imagingABSTRACT
Purpose: To evaluate the patient-reported outcomes of patients treated with commercially approved antibody-drug conjugates (ADC) reported in randomized controlled trials (RCT) published up to September 2023. Methods: A meta-analysis of 6430 patients from 12 randomized controlled trials was conducted. Results: No significant change was observed between the groups from baseline to end of treatment and end of follow-up, with a standardized mean difference of -0.08 (95% CI: -0.27-0.12) and 0.01 (95% CI: -0.11-0.12), respectively. Treatment with ADCs delayed the deterioration of patients' clinical condition compared with treatment with non-ADCs, with a hazard ratio of 0.78 (95% CI: 0.67-0.92). Conclusion: ADCs have a good correlation with delay of clinical deterioration in patients with cancer.
Subject(s)
Immunoconjugates , Neoplasms , Humans , Immunoconjugates/therapeutic use , Neoplasms/drug therapy , Quality of Life , Randomized Controlled Trials as TopicABSTRACT
Objectives: The aim of this study was to explore the effects of a virtual reality (VR)-based motivational reinforcement + desensitization intervention program on psychological craving and addiction memory in female methamphetamine (MA)-dependent young adults. Methods: We recruited 60 female MA-dependent young adults in a compulsory isolation drug rehabilitation facility in Sichuan Province, and randomly assigned them to intervention (mean age = 23.24 ± 2.06) and control groups (mean age = 23.33 ± 2.09). The intervention group received a VR-based motivational enhancement + desensitization intervention (total of eight sessions over a 4-week period), while the control group received regular detoxification management during the same period. Assessments were conducted before, immediately after, and 1 month after the intervention, with a visual analogue scale (VAS) being used to assess subjective craving, electronic sphygmomanometer employed to measure physiological parameters, and the Addiction Memory Intensity Scale (AMIS) applied to assess addiction memory intensity. Results: Generalized estimating equation analysis showed significant main effects of group on changes in heart rate difference, systolic blood pressure difference, VAS and AMIS scores (all p < 0.01), and a significant time main effect on changes in diastolic blood pressure difference, VAS and AMIS scores (all p < 0.01), and a significant group × time interaction effect on changes in the difference values of three physiological parameters, VAS and AMIS scores (p < 0.01 or p < 0.05). After the intervention, the differences in three physiological parameters, and the VAS and AMIS scores, were significantly lower in the intervention than in the control group (all p < 0.05), and the difference between the two groups remained significant 1 month after the end of the intervention (both p < 0.01). VAS scores, heart rate difference, and diastolic blood pressure difference in the intervention group were significantly lower than baseline scores, both at the end of the intervention and 1 month thereafter (all p < 0.01); the systolic blood pressure difference in the intervention group was significantly lower at the end of the intervention than at baseline (p < 0.05); AMIS scores in the intervention group were significantly lower than the baseline scores 1 month after the end of the intervention (p < 0.01). Conclusion: Our VR-based motivational reinforcement + desensitization intervention program can effectively reduce psychological craving and physiological reactivity for drugs, and the intensity of addictive memories in female MA-dependent young adults, even after 1 month.
ABSTRACT
Background: The use of antibody-drug conjugates for the treatment of advanced-stage human epidermal growth factor receptor 2 (HER2)-low expression in breast cancer (BC) has shown prominent curative effects, which has led to increased academic interest. However, the role of HER2-low expression in the prognosis of BC remains controversial. Methods: We conducted a systematic search of the PubMed, Embase, and Cochrane library databases and several oncology conferences until 20 September 2022. We used fixed- and random-effects models to calculate odds ratio (OR) or hazard ratio (HR) with 95% confidence interval (CI) for overall survival (OS), disease-free survival (DFS), progression-free survival (PFS), and pathological complete response (pCR) rates. Results: Overall, 26 studies encompassing 677,248 patients were included in the meta-analysis. Patients with HER2-low BC showed significantly better OS than those with HER2-zero BC in the overall population (HR = 0.90; 95% CI: 0.85-0.97) and hormone receptor-positive population (HR = 0.98; 95% CI: 0.96-0.99), whereas no significant difference was observed in the OS of the hormone receptor-negative population (p > 0.05). In addition, there was no significant difference in the DFS of the overall and hormone receptor-negative population (p > 0.05), but better DFS than those with HER2-zero BC in the hormone receptor-negative population (HR = 0.96; 95% CI: 0.94-0.99). There was also no significant difference in the PFS of the overall population, hormone receptor-positive, and hormone receptor-negative population (p > 0.05). Patients with HER2-low BC had a lower pCR rate after neoadjuvant treatment than those with HER2-zero BC. Conclusions: Compared to patients with HER2-zero BC, those with HER2-low BC had better OS in the overall population and hormone receptor-positive population, DFS in hormone receptor-positive population and lower pCR in the overall population. The biological differences between HER2-low and HER2-zero BCs, particularly in hormone receptor-positive patients, and the relationship between HER2-low expression status and prognosis need to be explored further.
ABSTRACT
The report describes a 27-year-old female patient with amelogenesis imperfecta (AI) accompanied by nocturnal bruxism, who was treated with a combination of occlusal splint and full-mouth fixed prosthetic rehabilitation through follow-ups within 2 years. Soft splint protection, regular follow-up, and monitoring of carries are guaranteed to maintain a long-term curative effect.
ABSTRACT
OBJECTIVE: The effects of the staurosporine on contraction of self-assembled constructs and extracellular matrix syntheses of goat temporomandibular joint discs were investigated. METHODS: Goatâtemporomandibular joint disc cells were isolated andâcultured to P3, and 5.5×106 cells were combined with different concentrations of staurosporine (0, 0.1, 1, 10, 100 nmol·L⻹) in agarose wells and cultured for one week. The samples were frozen and sectioned. Safranin-O,â Picro-siriusâred andâimmunohistochemicalâstainingâwereâperformedâto observe the distributions of the extracellular matrix and the expression of alpha-smooth muscle actin (α-SMA). Enzyme linked immunosorbent assay (ELISA) and Blyscan kits were utilized to quan--titatively detect the contents of type â collagen (Colâ ) and glycosaminoglycans (GAGs). RESULTS: Each group of goat temporo-mandibular joint disc cells in the agarose wells were gathered to self-assemble into a disc-shaped base for 4 hours and then to gradually contract into a round shape. The Picro-sirius red staining was strong and indicated collagen distribution. The Safranin-O staining observed GAGs throughout the entire construct. The expression of Colâ âwas strongly posi-tive in the staurosporine groups; however, the expression of α-SMA was weak. Colâ and GAGs contents in the stau-rosporine groups were greater than that of the control group, especially in the 10 nmol·L⻹ group (P<0.01). CONCLUSIONS: Staurosporine has a certain effect on the shrinkage of self-assembled constructs; however, such effect is not prominent. Staurosporine contributes to the construction synthesis of extracellular matrix.