Thermophilic-mesophilic temperature phase anaerobic co-digestion compared with single phase co-digestion of sewage sludge and food waste.

Anaerobic co-digestion is an effective method for addressing the issue of a single substrate not being able to achieve optimal conditions for anaerobic digestion. By adjusting the mixture ratio of sewage sludge and food waste to achieve the optimal carbon to nitrogen ratio, the effectiveness of thermophilic-mesophilic temperature phase anaerobic co-digestion (TPAcD) was evaluated in comparison to single phase mesophilic anaerobic co-digestion (MAcD) and thermophilic anaerobic co-digestion (TAcD). The results indicated that TPAcD increased methane yield by 50.3% and 32.7% compared to MAcD and TAcD, respectively. The variation in VFA, pH, and ammonia nitrogen levels demonstrated that TPAcD combines the advantages of both MAcD and TAcD, with a higher hydrolysis rate in the early stage under thermophilic conditions (55 °C) and a suitable environment in the later stage under mesophilic conditions (35 °C). The kinetic parameters of anaerobic co-digestions also demonstrated that TPAcD performs better. Therefore, further research on TPAcD of sewage sludge and food waste is warranted due to its significant improvements in methane production rate, total methane yield, and system stability. Additionally, TPAcD contributes to reducing carbon emissions and supports the realization of "carbon neutrality".

MiR-199a targeting ROCK1 to affect kidney cell proliferation, invasion and apoptosis.

Renal cell carcinoma (RCC) is one of the three most common cancers of urinary tract cancer, accounting for 2-3% of all systemic cancers. Recent studies have found that miR-199a is lowly expressed in RCC, may act as a tumour suppressor gene to induce the occurrence of kidney cancer. In the present study, we investigated the role of miR-199a in the progression and metastasis of RCC. The results showed that miR-199a significantly downregulated in RCC and cell lines. Overexpression of miR-199a in RCC cell lines significantly inhibited cell proliferation, migration and invasion. Furthermore, the qRT-PCR and western blot results showed that miR-199a overexpression significantly downregulated ROCK-1 mRNA and protein levels. ROCK1 was identified as a target of miR-199a, and ectopic expression of miR-199a downregulated ROCK1 by direct binding to its 3' untranslated region. Together, these findings indicate that miR-199a acts as a tumour suppressor and its downregulation in tumour tissues may contribute to the progression and metastasis of RCC through a mechanism involving ROCK1, suggesting miR-199a as a potential new diagnostic and therapeutic target for the treatment of RCC.