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Research reported prevalence of post-traumatic stress disorder (PTSD) among prisoners varies between countries, with most studies based on Western samples. The trajectory of symptoms has also been controversial. Trauma can affect prisoners' emotions and their emotional regulation tends to be maladaptive.To examine changes in PTSD and psychiatric comorbidity among prisoners in China over time and to determine whether anger and self-concealment predicts later distress.In a longitudinal, prospective study, sentenced men in one prison in China were asked to complete a demographic page and several self-rating scales: the Post-traumatic Stress Diagnostic Scale, the General Health Questionnaire-28, the Clinical Anger Scale and the Self-Concealment Scale at baseline and at 6 and 12 months after the initial assessment.More than half of the 496 participating men were diagnosed with PTSD. For those completing the scales at each evaluation, PTSD-DS scores were significantly lower at baseline than at the 6-month and 1-year assessments. No significant differences were found between the two follow-up scores. There was no significant difference in psychiatric comorbidity between the three phases. At the cross-sectional level, after controlling for age and education level, PTSD, anger and self-concealment were associated with psychiatric comorbidity. At the prospective level, anger predicted PTSD 6 months and 1 year later. Self-concealment predicted psychiatric comorbidity over time.Among these prisoners the prevalence of chronic PTSD was far higher than in general population estimates. Early identification of aspects of coping styles is likely to help predict disorder trajectory and inform interventions. Early signs of anger were indicative of the chronic severity of trauma reactions, while the intention to hide distress was related to other later mental health problems.

Induction chemotherapy (IC) comprising docetaxel, cisplatin, and fluorouracil (TPF), combined with concurrent chemoradiotherapy (CCRT) effectively improves the survival rate of locally advanced nasopharyngeal carcinoma (LA-NPC). Selecting patients whose risk of tumor recurrence and metastasis is high and the appropriate chemotherapy intensity is a concern. We combined tumor-node-metastasis staging with the load of Epstein-Barr virus (EBV) after IC to select the individualized chemotherapy strength.The clinical data and prognostic factors of patients with stage III-IV LA-NPC treated with TPF IC combined with CCRT were analyzed retrospectively. The conventional treatment group received the standard three cycles TPF IC combined with CCRT. For the new treatment group, the cycles of IC were determined according to whether the EBV-DNA disappeared completely after a certain course of IC, if so, subsequent IC was stopped and the chemoradiotherapy stage was entered. Propensity score matching (PSM) was performed at a ratio of 1:1 to balance baseline characteristics. Survival outcomes and adverse events between the conventional treatment group and the new method treatment group were compared.The study included 256 patients, among whom 192 were matched successfully into 96 pairs. The patients were followed up for a median of 51 months. The proportions of patients receiving three, two, and one cycle of IC after PSM in the routine and new treatment cohorts were 93.8%, 3.1%, 3.1% versus 21.9%, 49.0%, 24.0%, respectively. However, their 3-year distant metastasis-free survival, local recurrence-free survival, progression-free survival, and overall survival did not differ significantly. The incidence of grade 3-4 neutropenia toxicity in CCRT decreased significantly in patients receiving the new treatment method compared with that in the conventional treatment group (p = 0.026).Combining TNM stage and EBV-DNA load after IC to determine the courses of IC in patients with LA-NPC did not alter the curative effect but decreased toxicity.

Paclitaxel (PTX) has previously been used to treat tumours of various tissue origins, such as lung, breast, ovarian, prostate cancers and leukemia. PTX‐induced apoptosis is associated with p38 mitogen‐activated protein kinase (p38 MAPK), extracellular signal‐regulated kinase (ERK), nuclear factor‐kappa B (NF‐κB) and c‐Jun N‐terminal kinase or stress‐activated protein kinase (JNK/ SAPK) pathways. Transforming growth factor‐beta‐activated kinase 1 (TAK1) and TAK1‐binding protein 1 (TAB1) play an important role in cell apoptosis through the p38, ERK, NF‐κB and JNK signal transduction pathways. To investigate the role of TAK1 in PTX‐induced cell apoptosis, we treated HEK293 and 8305C cells with 0–20 µm PTX for 6, 12 or 24 h. To investigate whether TAK1 can cooperate with PTX for cancer treatment, we transfected cells with TAK1, TAB1 or control plasmid and treated them with PTX (3–10 µm) for 9–24 h. Apoptosis rates were analysed by flow cytometry (Annexin V/PI). Endogenous TAK1 and TAB1, caspase‐7 cleavage, poly ADP‐ribose polymerase (PARP) cleavage, Bcl‐xL level, phospho‐p44/42, phospho‐JNK and phospho‐p38 were detected by western blot. We show that in HEK293 and 8305C cells, PTX enhanced the endogenous TAK1/TAB1 level and induced cell apoptosis in a dose‐ and time‐dependent manner. Upon TAK1 overexpression in HEK293 cells treated with PTX, apoptosis rate, JNK phosphorylation and PARP cleavage increased contrary to heat‐shocked or untreated cells. CRISPR editing of the tak1 gene upon PTX treatment resulted in lower phospho‐JNK and PARP cleavage levels than in cells transfected with the control or the TAK1‐ or TAB1 + TAK1‐containing plasmids. TAK1‐K63A could not induce JNK phosphorylation or PARP cleavage. We conclude that PTX induces HEK293 and 8305C cell apoptosis through the TAK1–JNK activation pathway, potentially highlighting TAK1’s role in chemosensitivity., Paclitaxel induces HEK293 and 8305C cell apoptosis through the Transforming growth factor‐beta‐activated kinase 1 (TAK1)–c‐Jun N‐terminal kinase (JNK) activation pathway. Paclitaxel increases endogenous TAK1 and TAK1‐binding protein 1(TAB1) levels in HEK293 and 8305C cells in a dose‐ and time‐dependent manner. TAK1 and TAB1 complex induced JNK activation through phosphorylation, which leads to inhibition of Bcl‐xL.