Management of Acute Cerebral Infarction by Intravenous Thrombolysis with Recombinant T Cell Receptor and Plasminogen Activator and Association of Emergency Nursing Route in the Prognosis.

The purpose of this study is to determine the impact and prognosis of the emergency nursing approach in conjunction with the use of recombinant T cell receptors and plasminogen activators in patients who have just had an acute stroke. In this study, 100 patients were randomly selected that were equally divided into experimental and control groups. The period of hospital admission, the results of the Montreal Cognitive Assessment (MoCA) and the Mini-mental State Examination (MMSE), the results of the Glasgow Outcome Scale (GOS), and the results of the Activities of Daily Living were all analysed before and after the intervention.. Both the amount of time it took to get a diagnosis after being admitted and the amount of time it took to receive specialised therapy after receiving a diagnosis were significantly reduced in the observation group (both P values less than 0.05). At one month after discharge, the scores of ADL, MoCA, MMSE, and GOS rose in both groups, with more significant changes occurring in the observation group (all P<0.05). This was due to the fact that ADL scores declined while scores for MoCA, MMSE, and GOS increased. The percentage of people who were disabled in the observation group was significantly lower than the percentage in the control group (P<0.05).  Including emergency, nursing might drastically reduce the time it takes for patients with acute stroke to be admitted and begin receiving specialised care.

The ICU Is Becoming a Main Battlefield for Severe Maternal Rescue in China: An 8-Year Single-Center Clinical Experience.

OBJECTIVES: To review the characteristics of and to identify the reasons for severe maternal admissions to the ICU. DESIGN: This was an analytical, observational, open, and retrospective study. SETTING: In our ICU. PATIENTS: A total of 487 severe maternal cases were reviewed during the 8-year study period of January 2009 to December 2016. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: A total of 487 severe maternal cases (12.6%) among the 3,867 patients admitted to ICU were reviewed. Of these, 361 patients were admitted for obstetric reasons, mainly pregnancy-induced hypertension (58.7%) and postpartum hemorrhage (36.8%). The remaining 126 patients were admitted for nonobstetric reasons, including cardiac-related disease (31.0%), immune-related disease (24.6%), and sepsis (20.6%). A total of 249 patients experienced combined comorbidities: the most common was a scarred uterus (100 patients; 40.2%), followed by endocrine-related disease (25.3%), immune-related disease (21.3%), and cardiac-related disease (18.1%). Central venous insertion (90.6%) was the most common intervention, followed by arterial catheter insertion (33.7%), mechanical ventilation (11.7%), blood purification (5.7%), and invasive hemodynamic monitoring (3.7%). Nine patients died during the study period, of which the death of four could have been avoided. CONCLUSIONS: The number of severe maternal cases has increased annually in our ICU. Although obstetric causes remained the most common reason for admission, the nonobstetric causes and basic complications were too complex, dangerous, and beyond the reach of the obstetrician with regard to monitoring and treatment. We call for a multidisciplinary team mainly composed of ICU staff to improve severe maternal outcomes.

Mitochondrial tRNA mutation with high-salt stimulation on cardiac damage: underlying mechanism associated with change of Bax and VDAC.

Mitochondrial transfer RNA (tRNA) mutation with high-salt stimulation can cause high blood pressure. However, the underlying mechanisms remain unclear. In the present study, we examined the potential molecular mechanisms of cardiac damage caused by mitochondrial tRNA mutation with high-salt stimulation in spontaneously hypertensive rats (SHR). Unanesthetized, 44-wk-old, male, SHR were divided into four groups: SHR, SHR with high-salt stimulation for 8 wk (SHR + NaCl), SHR carrying tRNA mutations (SHR + M), and SHR + M with high-salt stimulation for 8 wk (SHR + M + NaCl). Healthy Wistar-Kyoto (WKY) rats were used as controls. Left ventricular mass and interventricular septum were highest in the SHR + M + NaCl group (P < 0.05), while ejection fraction was lowest in the SHR + M + NaCl group (P < 0.05). Hematoxylin and eosin staining showed myocardial cell hypertrophy with interstitial fibrosis and localized inflammatory cell infiltration, in the hypertensive groups, particularly in the SHR + M + NaCl group. Electron microscopy showed different degrees of mitochondrial cavitation in heart tissue of the hypertensive groups, which was highest in the SHR + M + NaCl group. In hypertensive animals, levels of reactive oxygen species were highest in the SHR + M + NaCl group (P < 0.05). Expression of the voltage-dependent anion channel (VDAC) and the apoptosis regulator Bax were highest in the SHR + M + NaCl group (P < 0.05), which also showed evidence of VDAC and Bax colocalization (P < 0.05). Overall, these data suggest that mitochondrial tRNA mutation with high-salt stimulation can aggravate cardiac damage, potentially because of increased expression and interaction between Bax and VDAC and increased reactive oxygen species formation and initiation of apoptosis.

Voltage-dependent anion channel (VDAC) is involved in apoptosis of cell lines carrying the mitochondrial DNA mutation.

BACKGROUND: The mitochondrial voltage-dependent anion channel (VDAC) is increasingly implicated in the control of apoptosis. We have studied the effects the mitochondrial DNA (mtDNA) tRNAIle mutation on VDAC expression, localization, and apoptosis. METHODS: Lymphoblastoid cell lines were derived from 3 symptomatic and 1 asymptomatic members of a family with hypertension associated with the A4263G tRNAIle mutation as well as from control subjects. Mitochondrial potential (DeltaPsim) and apoptosis were measured by flow cytometry; co-localization of VDAC and Bax was evaluated by confocal microscopy. RESULTS: Expression of VDAC and Bax in mtDNA cell lines was found to be increased compared to controls, while expression of the small conductance calcium-dependant potassium channel (sKCa) was unchanged. Confocal imaging revealed co-localization of VDAC/Bax on the outer mitochondrial membrane of A4263G cell lines but not from controls. Flow cytometry indicated that the mitochondrial potential was decreased by 32% in mutated cells versus controls while rates of apoptosis were increased (P < 0.05). The difference was attenuated by Cyclosporin A (CsA, 2 muM), a blocker of VDAC. CONCLUSION: We conclude that increased expression of mitochondrial VDAC and subcellular co-localization of VDAC/Bax increases mitochondrial permeability and apoptosis in cell lines carrying the mtDNA tRNAIle A4263G mutation.