Perineal resuturing versus conservative treatment for dehisced perineal wounds and episiotomies: a systematic review and meta-analysis.

INTRODUCTION AND HYPOTHESIS: Perineal wound dehiscence is associated with complications, such as infections, perineal pain, dyspareunia, and altered sexual function, that severely affects women's health. Currently, few studies have examined secondary repair of first- and second-degree perineal wound dehiscence and episiotomies, and there is currently no consensus on the optimal treatment option for dehisced perineal wounds. The objective was to evaluate whether resuturing or conservative treatment of first- and second-degree dehisced perineal wounds and episiotomies is the optimal treatment modality in terms of postoperative healing time and other secondary outcomes. METHODS: A systematic literature search was carried out using PubMed, Embase, and Cochrane databases. All included studies were evaluated using the SIGN methodology checklist, with the purpose of assessing the study quality. RESULTS: Three randomized controlled trials were included. Only two small sample-sized studies presented data regarding healing time for both the resuturing and the conservative treatment groups. However, no significant difference was found between the two groups at 4-6 weeks' healing time (RR 1.16, 95% CI 0.53-2.52). One study found that women being resutured experienced a significantly reduced healing time and higher satisfaction with the appearance of the wound healing at 3 months compared with the conservative treatment group. CONCLUSION: We found no significant differences in the healing time between the resuturing group and the conservative treatment group. However, the sample sizes of the studies were small. A well-designed, large, and prospective randomized controlled trial is needed to evaluate the optimal treatment modality for dehisced perineal wounds.

Inhibition of carnitine palmitoyl-transferase 1 is a potential target in a mouse model of Parkinson's disease.

Glucose metabolism is dysregulated in Parkinson's disease (PD) causing a shift toward the metabolism of lipids. Carnitine palmitoyl-transferase 1A (CPT1A) regulates the key step in the metabolism of long-chain fatty acids. The aim of this study is to evaluate the effect of downregulating CPT1, either genetically with a Cpt1a P479L mutation or medicinally on PD using chronic rotenone mouse models using C57Bl/6J and Park2 knockout mice. We show that Cpt1a P479L mutant mice are resistant to rotenone-induced PD, and that inhibition of CPT1 is capable of restoring neurological function, normal glucose metabolism, and alleviate markers of PD in the midbrain. Furthermore, we show that downregulation of lipid metabolism via CPT1 alleviates pathological motor and non-motor behavior, oxidative stress, and disrupted glucose homeostasis in Park2 knockout mice. Finally, we confirm that rotenone induces gut dysbiosis in C57Bl/6J and, for the first time, in Park2 knockout mice. We show that this dysbiosis is alleviated by the downregulation of the lipid metabolism via CPT1.

Downregulating carnitine palmitoyl transferase 1 affects disease progression in the SOD1 G93A mouse model of ALS.

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease characterized by death of motor neurons. The etiology and pathogenesis remains elusive despite decades of intensive research. Herein, we report that dysregulated metabolism plays a central role in the SOD1 G93A mouse model mimicking ALS. Specifically, we report that the activity of carnitine palmitoyl transferase 1 (CPT1) lipid metabolism is associated with disease progression. Downregulation of CPT1 activity by pharmacological and genetic methods results in amelioration of disease symptoms, inflammation, oxidative stress and mitochondrial function, whereas upregulation by high-fat diet or corticosterone results in a more aggressive disease progression. Finally, we show that downregulating CPT1 shifts the gut microbiota communities towards a protective phenotype in SOD1 G93A mice. These findings reveal that metabolism, and specifically CPT1 lipid metabolism plays a central role in the SOD1 G93A mouse model and shows that CPT1 might be a therapeutic target in ALS.