Therapeutic strategies for retention of cranioplasty titanium mesh after mesh exposure.

BACKGROUND: Titanium mesh exposure after cranioplasty is a possible complication and is usually managed by mesh removal and flap transfer, but the advantages of the rigid prosthesis are then lost. This study aimed to present our experience with negative pressure wound therapy combined with soft tissue dilation for retaining the titanium mesh in patients with mesh exposure after cranioplasty. METHODS: This retrospective study included patients treated between 01/2016 and 05/2019 at the Jiangyin Hospital Affiliated to Southeast University School of Medicine. The wound was cleaned, and a cystic space was created for the tissue dilator, which was used with a self-designed negative pressure dressing. After the target dilation was achieved, the repair was conducted while retaining the titanium mesh. RESULTS: Eight patients were included (seven males and one female; 53.6 ± 8.8 (range, 43-65) years of age). The exposed mesh area ranged from 1 × 1 to 4 × 5.5 cm. The thinning scalp area around the exposed mesh ranged from 3.6 × 3.8 to 4 × 5.5 cm. Five patients had positive wound cultures and received sensitive antibiotics. The dilator embedding time was 20-28 days. The time of negative pressure wound therapy was 25-33 days. The hospital stay was 30-41 days. Primary wound healing was achieved in all eight patients. There were no signs of recurrence after 6-18 months of follow-up. The cranial CT scans were unremarkable. CONCLUSIONS: Negative pressure wound therapy combined with soft tissue dilation for exposed titanium mesh after cranioplasty might help retain the titanium mesh.

Understanding the molecular association between hyperkalemia and lung squamous cell carcinomas.

BACKGROUND: Previous studies indicated a strong association between hyperkalemia and lung squamous cell carcinomas (LSCC). However, the underlying mechanism is not fully understood so far. METHODS: Literature-based data mining was conducted to identify genes, molecule, and cell processes linked to both hyperkalemia and LSCC. Pathway analysis was performed to explore the interactive network, common-target network, and common-regulator network for both disorders. Then, a mega-analysis using 11 independent LSCC RNA expression datasets (358 LSCCs and 278 healthy controls) was performed to test the hypothesis that genes influencing hyperkalemia may also play roles in LSCC. RESULTS: There was a significant overlap between the genes implicated with both diseases (20 genes, p-value = 4.98e-15), which counts for 16% of all hyperkalemia genes (125 genes). Network analysis identified 12 molecules as common targets for hyperkalemia and LSCC, and 19 molecules as common regulators. Moreover, 19 molecules were identified within an interactive network, through which hyperkalemia and LSCC could exert influence on each other. In addition, meta-analysis identified one hyperkalemia promoter, SPP1, as a novel contributor for LSCC (LFC = 2.64; p-value = 2.81e-6). MLR analysis suggests geographical region as an influential factor for the expression levels of SPP1 in LSCC patients (p value = 0.036, 0.054). CONCLUSION: Our results showed that there was a common molecular basis for the pathology of both hyperkalemia and LSCC, and that genes promoting hyperkalemia might also play roles in the development of LSCC. However, this study did not suggest hypercalcemia as a casual factor for LSCC.

Spatial patterns of intrinsic neural activity in depressed patients with vascular risk factors as revealed by the amplitude of low-frequency fluctuation.

To investigate spatial patterns of intrinsic neural activity of depressed patients with vascular risk factors using resting-state functional magnetic resonance imaging (fMRI) and to examine the relationship between regional activity abnormalities and symptom severity factor, we analyzed spatial patterns of spontaneous brain activity in 19 depressed patients with vascular risk factors and 18 healthy subjects. Intrinsic brain activity was measured by the amplitude of low-frequency fluctuations (ALFF) of the resting-state blood oxygen level dependent signal. Depressed patients with vascular risk factors showed decrease in ALFF in the limbic-cortical-striatal-pallidal-thalamic circuit. Specifically, the altered ALFF values (i.e., left insula and right superior frontal gyrus) were significantly correlated with depression severity in the depressed group. In addition, higher ALFF values in the right middle temporal gyrus and right superior temporal gyrus were observed in depressed patients with vascular risk factors. Our findings reveal distinct functional patterns of abnormal brain activity in depressed patients with vascular risk factors and have implications for the understanding of the pathophysiology of this understudied population.