Impact of continuity of care based on Triangle theory on nutritional status of patients after pancreatic cancer surgery: a retrospective study.

OBJECTIVE: To evaluate the impact of Triangle theory-based continuity of care on postoperative malnutrition in pancreatic cancer patients. METHODS: We retrospectively analyzed the data from 184 patients with pancreatic cancer admitted to The Second People's Hospital of Lanzhou City from January 2020 to May 2023. Patients were divided into a control group receiving conventional care (n = 114) and a study group receiving Triangle theory-based care (n = 70). Postoperative nutritional status and prognosis were compared between the two groups. Nutritional indexes included serum total protein (STP), albumin (ALB), and hemoglobin (HB). Self-care ability was assessed using the Exercise of Self-care Agency (ESCA). Quality of life was measured using the Quality-of-Life Questionnaire for Pancreatic Cancer 26 (QLQ-PAN-26), and the incidence of malnutrition was evaluated using the Patient-Generated Subjective Global Assessment (PG-SGA). Multifactorial logistic regression was applied to analyze risk factors for malnutrition. RESULTS: At ten days post-operation, the study group showed significantly better nutritional levels (P < 0.05). After three months, the, study group also exhibited superior self-care ability and quality of life scores (all P < 0.001). The incidence of malnutrition was 42.39%. Independent risk factors for malnutrition included routine care (OR = 3.459), operation time ≥ 90 min (OR = 2.277), intraoperative bleeding ≥ 200 mL (OR = 2.590), postoperative day 1 ALB < 37.5 g/L (OR = 3.975), and HB < 95.5 g/L (OR = 6.068). CONCLUSION: Triangle theory-based continuity of care significantly improves nutritional status and quality of life in postoperative pancreatic cancer patients, demonstrating its potential for broader clinical use.

t-PA reduces ischemic impairment of blood-brain barrier by strengthening endothelium junction.

Cerebral ischemic stroke is one of the most prevalent diseases in senior individuals. Its therapeutical strategies include anticoagulation, thrombolysis and cell protection. Tissue-type plasminogen activator (t-PA) that interacts with thrombin for the lysis of thrombosis is widely used to treat stroke patients in early stage. The mechanism of action of t-PA is not clear. Here, we report a novel role of t-PA in protecting blood-brain barrier and its potential mechanisms. In a model of the blood-brain barrier with human umbilical vascular epithelium cells, we found that t-PA in low concentrations prevented the impairment of the blood-brain barrier as a result of oxygen and glucose deprivation. This protection was fulfilled by strengthening the junctions among vascular endothelia and by upregulating the productions of vascular endothelium growth factor and of zonula occludens-1. Therefore, t-PA may strengthen the junctions of vascular endothelia in the blood-brain barrier to improve the microenvironment of brain cells and, in turn, the outcome of stroke patients.

An impairment of cortical GABAergic neurons is involved in alkalosis-induced brain dysfunctions.

Acid-base imbalance leads to pathological cognition and behaviors in the clinical practices. In the comparison with acidosis, the cellular mechanisms underlying alkalosis-induced brain dysfunction remain unclear. By using electrophysiological approach, we investigated the influences of high extracellular pH environment on cortical GABAergic neurons in terms of their responsiveness to synaptic inputs and their ability to produce action potentials. Artificial cerebral spinal fluid in high pH impairs excitatory synaptic transmission and spike initiation in cortical GABAergic neurons. The alkalosis-induced dysfunction of GABAergic neurons is associated with the decrease of receptor responsiveness and the increases of spike refractory periods and threshold potentials. Our studies reveal that alkalosis impairs cortical GABAergic neurons and subsequently deteriorate brain functions. The molecular targets for alkalosis action include glutamate receptor-channels and voltage-gated sodium channels on GABAergic neurons.

Impact of migraine attacks on the blood-brain barrier.

BACKGROUND: Cortical spreading depression can cause migraine attack, and up-regulate matrix metalloproteinase-9 (MMP-9) expression in animal. This study aimed to determine the impact on the structure and function of the blood-brain barrier by measuring plasma MMP-9 levels in patients at the acute and late stages of migraine attacks in order to elucidate the pathological mechanisms involved. METHODS: We recruited a case-control cohort of 38 adult migraine patients and 20 age- and gender-matched healthy control subjects. Five milliliter blood samples were collected at the acute and late stages of migraine (days 1 - 7), and also from the control subjects. Solid phase double antibody sandwich enzyme-linked immunosorbent assay was used to determine plasma MMP-9 levels. Statistical analysis was performed using the SAS version 9.1. RESULTS: Initial plasma MMP-9 levels of migraine patients were significantly higher than those of controls ((12.612 ± 0.016) µg/L vs. (6.069 ± 0.023) µg/L, respectively, P < 0.05). High MMP-9 expression was observed during days 1 - 6 of migraine attacks, with highest expression occurring on day 3 ((17.524 ± 0.035) µg/L). During attacks, MMP-9 levels were similar in migraine patients with and without aura (P > 0.05); in addition, levels were not correlated with degree of headache pain (P > 0.05). CONCLUSIONS: We hypothesize that migraine could lead to increased plasma MMP-9 levels resulting in blood-brain barrier damage. MMP-9 levels increase during days 1 - 6 of migraine attacks, peaking on day 3. Therefore, MMP-9 could be used as a biological marker to guide treatment of migraine attacks.