Notes

Affect involving carcinoma within situ in emergency regarding patients dealt with by adjuvant radiation treatment soon after cystectomy.
INTRODUCTION Although various treatment options for hidrocystomas have been described, the comparative efficacy of these treatments is poorly understood. METHODS We conducted a systematic review of all articles describing the treatment of hidrocystomas. Treatment modalities were categorized as destructive surgical procedures, skin-directed therapies, systemic medical therapies, general measures, or combined. HPPE Patient and tumor characteristics, as well as response rate, recurrence rate, and adverse effects, were extracted from each article. RESULTS A total of 94 articles involving 192 patients and 255 unique treatment events were included in the final analysis. Destructive surgical procedures had an overall response rate and recurrence rate of 92.9% and 10.8%, respectively. Skin-directed therapies had an overall response rate of 72.6%. The overall response rate to systemic medical therapies was 71.4%. Solitary hidrocystomas were primarily treated with destructive surgical procedures, including excision, which was associated with a 4.7% recurrence rate. Multiple hidrocystomas were successfully treated with a variety of therapies, including destructive surgical procedures and skin-directed therapies requiring ongoing or repeated therapy. CONCLUSIONS Excision has the highest efficacy for solitary hidrocystomas. A number of therapies have shown efficacy for multiple hidrocystomas, including lasers, intracystic trichloroacetic acid, intracystic hypertonic glucose, topical and oral anticholinergics, and botulinum toxin. Aluminum chloride is associated with a low response rate. Larger comparative studies are needed to further evaluate the optimal treatments for solitary and multiple hidrocystomas.Aim Noninvasive assessments of C-reactive protein (CRP) in stress contexts have seldom been compared. This study evaluated CRP response to acute social stress as measured in saliva and dried blood spot (DBS). Materials & methods African Americans (N = 118; mean age = 32 years) participated in a laboratory-based social-evaluative stressor task. Six saliva samples taken before, during and after were assayed for salivary CRP. DBS measurements of CRP were taken alongside saliva at the first and last collection. Results Salivary and DBS CRP were modestly positively associated with one another at baseline, and only salivary CRP increased in response to the stressor task. Conclusion Noninvasive measures of CRP reactivity may be only moderately related to one another in stress reactivity contexts.Patient engagement in clinical research refers to the involvement of patients beyond the role of research subject. To date, the goals of patient engagement have not been clearly defined for each stage of the research enterprise, which, when viewed broadly, encompasses stages such as setting research priorities, interpreting and incorporating research results in clinical guidance, and translating study results into insurance coverage policies. This article presents a new framework for patient engagement by first describing the goals of patient engagement at each stage of the research enterprise and then establishing how to prioritize the types of patient expertise that are needed to achieve these goals.AIMS Traumatic brain injury (TBI) is a major cause of disability and death, and a better understanding of the underlying mechanisms of mitochondrial dysfunction will provide important targets for preventing damage from neuronal insults. Phosphoglycerate mutase 5 (PGAM5) is localized to the mitochondrial outer-inner membrane contact sites, and the PGAM5-Drp1 pathway is involved in mitochondrial dysfunction and cell death. The purpose of this project was to evaluate the effects of PGAM5 on neuronal injury and mitochondrial dysfunction. RESULTS PGAM5 was overexpressed in mice subjected to TBI and in primary cortical neurons injured by mechanical equiaxial stretching. PGAM5 deficiency alleviated neuroinflammation, blocked Parkin, PINK1, and Drp1 translocation to mitochondria and abnormal phosphorylation of Drp1, mitochondrial ultrastructural changes, and nerve malfunction in TBI mouse model. PGAM5-shRNA reduced Drp1 translocation and activation, including dephosphorylation of p-Drp1 on Ser622 (human Drp1 Ser616) and phosphorylation of Drp1 on Ser643 (human Drp1 Ser637). The levels of inflammatory cytokines, the degree of mitochondrial impairment (mitochondrial membrane potential, ADP/ATP, AMP/ADP, antioxidant capacity), and neuronal injury in stretch-induced primary cortical neurons were reduced by blocking expression of PGAM5. The inhibition of PGAM5 is neuroprotective via attenuation of Drp1 activation, similar to that achieved by Mdivi1-mediated Drp1 inhibition. Innovation and Conclusion Our findings demonstrate the critical role of PGAM5 in progression of neuronal injury from TBI via Drp1 activation (dephosphorylation of p-Drp1 on Ser622 and phosphorylation of Drp1 on Ser643)-mediated mitochondrial dysfunction. The data may open a window for developing new drugs to prevent the neuropathology of TBI.AIMS High-fat diet (HFD)-induced insulin resistance (IR) impairs skeletal muscle mitochondrial biogenesis and functions, adversely affecting human health and lifespan. Vitamin K2 (VK2) has a beneficial role in improving insulin sensitivity and glucose metabolism. However, the underlying molecular mechanisms of VK2 on insulin sensitivity have not been well established. We investigated VK2's modulation of mitochondrial function to protect against IR in mice and cell models. RESULTS VK2 supplementation could effectively ameliorate the development of IR by improving mitochondrial function in both HFD-fed mice and PA-exposed cells. We revealed for the first time that HFD-caused mitochondrial dysfunction could be reversed by VK2 treatment. VK2 enhanced the mitochondrial function by improving mitochondrial respiratory capacity, increasing mitochondrial biogenesis and the enzymatic activities of mitochondrial complexes through SIRT1 signaling. The benefits of VK2 were abrogated in C2C12 transfected with SIRT1 siRNA but not in C2C12 transfected with AMPK siRNA. VK2 and SRT1720, a specific agonist of SIRT1, had the same effect on improving mitochondrial function via SIRT1 signaling. Thus, SIRT1 is required for VK2 improvement skeletal muscle. Furthermore, the beneficial effects of VK2 and GGOH both contribute to inhibited IR in skeletal muscle via SIRT1. INNOVATION These studies demonstrated a previously undiscovered mechanism by which VK2 alleviates IR in skeletal muscle by improving mitochondrial function via SIRT1. CONCLUSION Naturally occurring VK2 prevents IR by improving mitochondrial function through SIRT1 signaling. These results could provide a foundation to identify new VK2-based preventive and therapeutic strategies for IR.
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