The 16S rDNA polymerase chain reaction (PCR)-denaturing gradient gel electrophoresis (DGGE) and sequencing method has been demonstrated to be valuable in detecting pathogens in the blood of patients suffering from fever or neutropenia. However, its use in the diagnosis of neonatal late‑onset septicemia (LOS) has not yet been reported. The aim of the present study was to investigate the efficiency of this method in detection of the type of bacterial infection in neonatal LOS. Blood specimens from 60 neonates in whom LOS was suspected were collected. Fourteen culture positive blood samples and 24 spiked 'infected' blood samples were analyzed by the 16S rDNA PCR‑DGGE and sequencing method or by pathogen‑specific PCR. Only in 5 of the 14 cases did the results of 16S rDNA PCR‑DGGE and sequencing match with the results of blood culturing. In the other 9 cases, the blood culture failed to detect bacteria, such as Neisseria sp. and Moraxella sp., which were detected by 16S rDNA PCR‑DGGE and sequencing. Furthermore, the 16S rDNA PCR‑DGGE and sequencing failed to detect blood culture‑proven bacteria, such as Klebsiella pneumonia. A competitive inhibitory effect in 16S rDNA PCR amplification may lead to the discrepancy between pathogen‑specific PCR and spiked 'infected' blood samples. When a certain species of bacteria was detected by 16S rDNA PCR, the competitive inhibitory effect presented a higher sensitivity in detecting this species in the blood samples that contained bacterial DNA only from this species compared with the blood samples that were blended with other bacterial DNAs. In conclusion, 16S rDNA PCR‑DGGE and sequencing can detect a more comprehensive spectrum of pathogens than blood culture. However, the competitive inhibitory effect, which may lead to false negative results should be taken into consideration when the 16S rDNA PCR-DGGE and sequencing method is applied to the diagnosis of neonatal LOS.

Background/Objectives: Ketogenic diets (KDs), defined by very low carbohydrate and high fat content, are widely studied for obesity and metabolic disease. However, KD formulations vary from 60–95% fat, leading to inconsistent induction of ketogenesis and variable outcomes. The fat threshold required for sustained ketosis, and the tissue-specific programs that mediate KD efficacy, remain unclear. Methods: We evaluated multiple KD formulations (80–95% fat) in C57BL/6J wild-type (WT) and diet-induced obese (DIO) mice. Plasma, hepatic, and intestinal β-hydroxybutyrate (BHB) were measured together with expression of ketogenesis and fatty acid oxidation genes. Body weight, adipose distribution, and liver morphology were assessed under both direct feeding and therapeutic settings. Results: In WT mice, only diets exceeding 85% fat induced robust ketogenesis, reflected by elevated BHB and hepatic upregulation of Cd36, Cpt1a, Acat1, and Hmgcs2. Moderate KDs (80–85%) failed to trigger ketosis and resembled high-fat feeding. In obese mice, an 80% KD lowered fasting glucose without reducing body weight, whereas a 90% KD promoted systemic ketosis, weight loss, and adipose reduction. Interestingly, hepatic transcriptional programs for fatty acid oxidation and ketogenesis were suppressed under 90% KD despite elevated BHB, suggesting reliance on substrate availability and peripheral utilization. In contrast, intestinal Hmgcs2 was strongly induced in both WT and DIO mice, with Oxct1 upregulated only in obesity, indicating local ketone production and consumption. Conclusions: These findings identify > 85% dietary fat as a threshold for sustained ketosis and highlight distinct liver–intestine contributions, underscoring ketogenesis as the central driver of KD’s anti-obesity benefits.

The mechanism of avian navigation is an important question for global scientists. One of the most famous candidates is the radical pair mechanism (RPM), which shows that avian navigation is achieved by detecting the amount of products from chemical reactions, which exhibit different properties for singlet and triplet spin states. Based on the theory, we explore the amount of the the singlet recombination product by changing the coupling strength and direction of the magnetic field. The radical pair in our model is coupled with a Lipkin-Meshkov-Glick (LMG) bath, which proposes attractive results at quantum phase transition (QPT) point, especially when the magnetic field is parallel with the original direction of the pair. We find weakest navigation ability in QPT point according to one of our proposing methods. And we find invariant subspace in our Hamiltonian when the magnetic field is vertical to the plane of the radical pair and the bath, which will greatly speed up our calculation. Our results could help the exploration of the design principle of artificial avian navigation.