OBJECTIVE:To analyze the characteristics of carbapenem antibacterial drugs induced adverse drug reactions(ADR),and to provide foundation for reasonable drug use in the clinic.METHODS:Retried from CNKI and Wanfang database,106 literatures about carbapenem antibacterial drug-induced adverse drug reactions published from 2007 to 2012 were collected,involving 30 journals and 119 patients.Patient's sex,age,primary disease,drug involved,occurrence time of ADR,organs or system involved in ADR and clinical manifestation,and outcome were analyzed statistically.RESULTS:Among 119 patients,there were 76 male and 42 female patients,and one patient was not clear;highest incidence of ADR occurred in patients aged 61-80;respiratory,digestive,circulatory system diseases were main primary disease;carbapenem involved imipenem/cilastatin sodium,meropenem,biapenem;89.08% of patients suffered from ADR with more than 5 h administration;main ADR almost distributed in nerves,digestive and circulatory system;ADR of 94.12% of patients disappeared after withdrawal of the durgs.CONCLUSIONS:ADR should be paid more attention to in clinical practice to improve safety and effectiveness of drug use and reduce the occurrence of ADR.
The rapid growth of modern Internet applications demands ever-increasing transmission capacity and reduced latency in optical interconnect systems utilizing intensity modulation and direct detection (IM/DD). However, the intrinsic limitations of silica-based standard single-mode fiber (SMF) will ultimately be insufficient to meet these escalating demands. The nested antiresonant nodeless fiber (NANF), a newly designed hollow-core fiber, has garnered significant attention as a potential solution to these challenges. In this paper, we simultaneously address the issues of capacity and latency in a self-developed 20 km NANF-based four-level pulse amplitude modulation (PAM-4) IM/DD system. To mitigate the chromatic dispersion-induced power fading encountered in NANF, we implement effective compensation and fast equalization based on Tomlinson-Harashima precoding (THP) and a modified feedforward equalization with parallel multi-output (MFFE). Additionally, we measure the propagation latency in NANF using high-time-resolution entangled photon pairs. Experimental results demonstrate an achievement of beyond 200 Gb/s/λ in a PAM-4 IM/DD system operating in C-band over 20 km NANF transmission. Furthermore, the fast-computational equalizer reduces the processing time by 64.6% compared to conventional FFE. In terms of latency, the NANF demonstrates a 31.72% reduction in time delay compared to SMF, offering a viable pathway for future high-capacity and low-latency fiber-optic systems.
Abstract Background Inflammatory reaction plays a key role in the pathogenesis of hypoxic-ischemic encephalopathy (HIE) in neonates. Microglia are resident innate immune cells in the central nervous system and are profoundly involved in neuroinflammation. Studies have revealed that atorvastatin exerts a neuroprotective effect by regulating neuroinflammation in adult animal models of brain stroke and traumatic brain injury, but its role regarding damage to the developing brain remains unclear. This study aimed to clarify the effect and mechanism of atorvastatin on the regulation of microglia function in neonatal hypoxic-ischemic brain damage (HIBD). Methods The oxygen glucose deprivation (OGD) of microglia and neonatal rat HIBD model were established. Atorvastatin, recombinant sclerostinprotein (SOST), and XAV939 (degradation of β-catenin) were administered to OGD microglia and HIBD rats. The pathological changes of brain tissue, cerebral infarction volume, learning and memory ability of rats, pro-inflammatory (CD16 + /Iba1 + ) and anti-inflammatory (CD206 + /Iba1 + ) microglia markers, inflammation-related indicators (Inos, Tnfα, Il6, Arg1, Tgfb, and Mrc1), and Wnt/β-catenin signaling molecules were examined. Results Atorvastatin reduced OGD-induced pro-inflammatory microglia and pro-inflammatory factors, while increasing anti-inflammatory microgliaand anti-inflammatory factors. In vivo, atorvastatin attenuated hypoxia-ischemia (HI)-induced neuroinflammation and brain damage. Mechanistically, atorvastatin decreased SOST expression and activatedthe Wnt/β-catenin signaling pathway, and the administration of recombinant SOST protein or XAV939 inhibited Wnt/β-catenin signaling and attenuated the anti-inflammatory effect of atorvastatin. Conclusions Atorvastatin promotes the pro-/anti-inflammatory phenotypic transformation of microglia via the Wnt/β-catenin pathway in HI neonatal rats. Atorvastatin may be developed as a potent agent for the treatment of HIE in neonates.
Nonalcoholic fatty liver disease (NAFLD) is characterized by lipid accumulation in the liver and associates with obesity, hyperlipidemia, and insulin resistance. NAFLD could lead to nonalcoholic steatohepatitis (NASH), hepatic fibrosis, cirrhosis, and even cancers. The development of therapy for NAFLD has been proven difficult. Emerging evidence suggests that liver X receptor (LXR) antagonist is a potential treatment for fatty liver disease. However, concerns about the cholesterol-increasing effects make it questionable for the development of LXR antagonists. Here, the overweight monkeys were fed with LXRβ-selective antagonist sophoricoside or LXRα/β dual-antagonist morin for 3 months. The morphology of punctured liver tissues was examined by H&E staining. The liver, heart, and kidney damage indices were analyzed using plasma. The blood index was assayed using complete blood samples. We show that LXRβ-selective antagonist sophoricoside and LXRα/β dual-antagonist morin alleviated lipid accumulation in the liver in overweight monkeys. The compounds resulted in higher plasma TC or LDL-c contents, increased white blood cell and lymphocyte count, and decreased neutrophile granulocyte count in the monkeys. The compounds did not alter plasma glucose, apolipoprotein A (ApoA), ApoB, ApoE, lipoprotein (a) (LPA), nonesterified fatty acid (NEFA), aspartate transaminases (AST), creatinine (CREA), urea nitrogen (UN), and creatine kinase (CK) levels. Our data suggest that LXRβ-selective and LXRα/β dual antagonism may lead to hypercholesterolemia in nonhuman primates, which calls into question the development of LXR antagonist as a therapy for NAFLD.
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