Experience of multidisciplinary medical teams on humanistic palliative care in oncology wards: a descriptive qualitative study in Southern China.

OBJECTIVES: This study aimed to explore the experiences of multidisciplinary medical teams in implementing humanistic palliative care within the oncology ward. DESIGN: Purposive and snowball sampling methods were used in this qualitative study, which involved conducting semistructured interviews to gather personal experiences from members of multidisciplinary medical teams providing humanistic palliative care in the oncology ward. SETTING: The research was conducted in the oncology ward of a tertiary hospital located in Foshan, China. PARTICIPANTS: Participants included 4 doctors, 12 nurses and 2 medical social workers who form the multidisciplinary medical team responsible for delivering humanistic palliative care to patients with cancer in oncology wards. RESULTS: Phenomenological qualitative analysis yielded 3 main themes and 9 subthemes. The identified themes were as follows: (1) conceptual change, (2) concrete actions and (3) facilitators and barriers to the implementation of humanistic palliative care. CONCLUSION: The findings suggest a need for strengthening humanistic consciousness among multidisciplinary palliative care teams working in oncology wards, although there has been a gradual improvement in humanistic care behaviours. Furthermore, facilitators and barriers coexist in the implementation of humanistic palliative care. Efforts should be directed towards refining mechanisms that promote humanistic palliative care, fostering the enthusiasm of healthcare professionals, conducting systematic training to enhance their humanistic care abilities and striving for improvements in the quality of medical services for the benefit of both patients and their families.

The TRIM37 variants in Mulibrey nanism patients paralyze follicular helper T cell differentiation.

The Mulibrey (Muscle-liver-brain-eye) nanism caused by loss-of-function variants in TRIM37 gene is an autosomal recessive disorder characterized by severe growth failure and constrictive pericarditis. These patients also suffer from severe respiratory infections, co-incident with an increased mortality rate. Here, we revealed that TRIM37 variants were associated with recurrent infection. Trim37 FINmajor (a representative variant of Mulibrey nanism patients) and Trim37 knockout mice were susceptible to influenza virus infection. These mice showed defects in follicular helper T (TFH) cell development and antibody production. The effects of Trim37 on TFH cell differentiation relied on its E3 ligase activity catalyzing the K27/29-linked polyubiquitination of Bcl6 and its MATH domain-mediated interactions with Bcl6, thereby protecting Bcl6 from proteasome-mediated degradation. Collectively, these findings highlight the importance of the Trim37-Bcl6 axis in controlling the development of TFH cells and the production of high-affinity antibodies, and further unveil the immunologic mechanism underlying recurrent respiratory infection in Mulibrey nanism.

Lactate anions participate in T cell cytokine production and function.

After antigen stimulation, T cells preferentially increase aerobic glycolysis to meet the bioenergetic and biosynthetic demands of T cell activation, proliferation, and effector functions. Lactate, a by-product of glycolysis, has been reported to function as an important energy source and signaling molecule. Here, we found that lactate anions are involved in cytokine production in T cells after TCR activation. During ex vivo T cell activation, the addition of excess sodium lactate (NaL) increased the production of cytokines (such as IFNγ/IL-2/TNFα) more than the addition of sodium chloride (NaCl). This enhanced cytokine production was dependent on TCR/CD3 activation but not CD28 activation. In vivo, NaL treatment inhibited tumour growth in subcutaneously transplanted tumour models in a T cell-dependent manner, which was consistent with increased T cell cytokine production in the NaL treatment group compared to the NaCl treatment group. Furthermore, a mechanistic experiment showed that this enhanced cytokine production was regulated by GAPDH-mediated post-transcriptional regulation. Taken together, our findings indicate a new regulatory mechanism involved in glycolysis that promotes T cell function.