Investigation of gauze and medical bottle co-pyrolysis on the product formation, reactivity, and reaction pathway of char, liquid oil, and gas.

Effective in-site treatment of medical waste has become a weak link in hospitals. Pyrolysis technology is a treatment method for medical waste that can enable rapid disposal in hospital settings and relieve environmental pressure, while also producing high-value products and reducing disposal costs. In this work, the effects of feedstock ratio and temperature on product yield and components of gauze (GA) and medical bottles (MB) co-pyrolysis have been investigated. The higher yield of solid products was obtained by co-pyrolysis of GA and MB at 400 ℃. With the addition of MB and an increase in temperature for the co-pyrolysis of GA and MB in a similar ratio, the pyrolysis oil and gas yields gradually increased. According to GC-MS analysis, co-feeding 75% MB to GA improved the alcohol content from 33.21% to a maximum yield of 59.8% at a pyrolysis temperature of 700 ℃. The content of aliphatic hydrocarbon reached 38.68% when the pyrolysis temperature and MB addition ratio were 700 °C and 75%, respectively. The GC data shows that the main gas components of co-pyrolysis of GA/MB were CH4 and H2, while the pyrolysis of pure GA or MB resulted in CO or CO2. Additionally, the solid carbon products obtained have an excellent pore structure. This strategy can benefit medical waste control and resource utilization for the low-cost disposal of medical waste and the acquisition of high-value resource products.

Incidence and risk factors for febrile neutropenia of patients with diffuse large B-cell lymphoma receiving R-CHOP-21 in China.

OBJECTIVE: Febrile neutropenia (FN) is a serious complication of patients with diffuse large B-cell lymphoma (DLBCL) receiving R-CHOP-21. The prophylactic use of granulocyte colony-stimulating factors (G-CSFs) can significantly reduce the risk of FN. International guidelines recommend G-CSFs for patients receiving chemotherapy with FN risk of 20% or 10 to 20% with defined risk factors. However, there are few studies on the incidence and risk factors of FN in patients with DLBCL receiving R-CHOP-21, especially in patients without primary G-CSF prophylaxis. METHODS: We conducted a retrospective analysis for the clinical data of 103 patients with DLBCL who underwent first R-CHOP-21 without primary G-CSF prophylaxis. The objective of the assessment was the incidence and risk factors of FN after the first chemotherapy cycle. RESULTS: After the first chemotherapy cycle, the incidence of FN was 20.4%. Multivariate analysis showed that age ≥ 65 years, bone marrow involvement, albumin < 35 g/L, and average relative dose intensity ≥ 80% were independent risk factors for FN. According to risk factors, we created a risk score system. The incidence of FN in the low-, intermediate- and high-risk groups was 5.6%, 17.2%, and 61.9%, respectively. CONCLUSION: Our data indicated that R-CHOP-21 itself is associated with a high-risk regiment for FN. We recommend that intermediate/high-risk patients should actively consider primary G-CSF prophylaxis to reduce the incidence of FN after chemotherapy.

PPARγ stimulates expression of L-type amino acid and taurine transporters in human placentas: the evidence of PPARγ regulating fetal growth.

Placental amino acid transporters and peroxisome proliferator-activated receptors (PPARs) have been implicated to placental development and therefore regulation of fetal growth. We analyzed the correlation between the expression of amino acid transporters and PPARs and investigated whether PPARs control the expression of amino acid transporters in placentas. It was found that protein expression of PPARγ and L-type amino acid transporter 1(LAT1) and 2 (LAT2) was decreased in small-for-gestational-age (SGA) placentas. LAT1, LAT2 and taurine transporter (TAUT) expression correlated to PPARγ level and birth weight. In cultured placental cells, PPARγ agonist stimulated LAT1 and LAT2 and TAUT, which was reversed by PPARγ siRNA. PPARγ up-regulation of LAT1 and TAUT was through specificity protein 1 (Sp-1) while stimulation of LAT2 expression was via induction of gene transcription. Our data suggest that PPARγ, SP-1, LAT1 and LAT2 in placentas are involved in control of fetal growth. PPARγ signaling pathway may be the therapeutic target for intrauterine growth restriction.

Reduced expression of 11ß-hydroxysteroid dehydrogenase type 2 in preeclamptic placentas is associated with decreased PPARγ but increased PPARα expression.

Placental 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD2) is reduced in pregnancies complicated with preeclampsia (PE). Peroxisome proliferator-activated receptors ß/δ (PPARß/δ) have been shown to suppress 11ß-HSD2 expression in human placental cells. Our objectives were to investigate whether the reduced 11ß-HSD2 expression is associated with the changes in PPARs in PE placentas, and whether PPARα and PPARγ affect 11ß-HSD2 expression in placental cells. PPARα and PPARß/δ mRNA and protein expression was increased, whereas PPARγ mRNA and protein expression was decreased in PE placentas. 11ß-HSD2 protein expression was inversely correlated with PPARß/δ in normal placentas but correlated positively with PPARγ and inversely to PPARα in PE placentas. In cultured placental cells, PPARα agonist inhibited, whereas PPARγ agonist stimulated, 11ß-HSD2 mRNA and protein expression and activity in a dose-dependent manner. Knockdown of retinoid X nuclear receptor α (RXRα) resulted in a loss of PPARγ effect but not PPARα effect on11ß-HSD2. The PPARα effect remained, but the PPARγ effect was lost in the presence of the translational inhibitor cycloheximide. PPARγ agonist dose-dependently stimulated specificity protein 1 (Sp-1) protein expression. Inhibition or knockdown of Sp-1 resulted in a loss of the effects of PPARα and PPARγ. The Sp-1 protein level was not correlated with 11ß-HSD2 and PPARs in normal placentas, whereas Sp-1 expression was correlated with 11ß-HSD2, PPARγ, and PPARß/δ in PE placentas. Our data indicate that 11ß-HSD2 expression can be modulated by PPARα and PPARγ in placental trophoblasts through Sp-1. Decreased 11ß-HSD2 expression in PE placenta might be associated with decreased PPARγ but increased PPARα expression.