Biomedical subjects
Publications and source records attributed to Zhihai Liu.
A simple method for coupling between a single-core single-mode fiber and a multicore single-mode fiber is proposed and demonstrated. An effective coupling approach is based on a process of standard splicing and tapering between the single-core single-mode fiber and the multicore single-mode fiber.
A novel fiber-optic in-fiber integrated Michelson interferometer has been proposed and demonstrated. It consists of a segment of two-core fiber with a mirrored fiber end. The sensing characteristics based on the two-core fiber bending, corresponding to the shift of the phase of the two-core in-fiber integrated Michelson interferometer, are investigated.
BACKGROUND: Growth hormone (GH) has been shown to increase mortality in critical illness, illustrating the need for better understanding of GH treatment. The neutrophil is a key mediator in producing organ injury following shock and trauma and is regulated by GH. Therefore, the purpose of the present study was to examine the effects of GH on circulating neutrophil activation and subsequent lung injury induced by sepsis in rats. MATERIALS AND METHODS: Sepsis was induced in male Wistar rats via cecal ligation and puncture (CLP). Recombinant human growth hormone (1 IU/kg) was given subcutaneously right after CLP with an additional injection at 12 h after CLP. CD11b expression and an oxidative burst of neutrophils were detected using flow cytometric analysis. Lung myeloperoxidase activity was determined as an index of tissue neutrophil accumulation. Lung microvascular injury was assessed by quantitating extravasation of Evan's blue dye into lung parenchyma. RESULTS: Growth hormone significantly increased sepsis-induced expression of CD11b and sepsis-induced circulating neutrophil activation. Also growth hormone increased neutrophil accumulation in lungs induced by sepsis. Lung microvascular injury was aggravated by growth hormone treatment in septic rats. CONCLUSIONS: It is worthwhile to rethink GH administration in critical illness and further studies are required to determine the safety and clinical benefits of GH administration in critical illness.
The purpose of this study was to examine the effects of growth hormone (GH) on nuclear factor kappa B (NF-kappaB) activation and organ injury induced by lipopolysaccharide (LPS) in rats. Male Wistar rats were divided into 6 groups treated with saline, LPS (5 mg/kg), LPS plus GH (0.5, 1.0, 2.0 mg/kg), or GH (2.0 mg/kg) alone for 2 or 4 hr. NF-kappaB activity and I-kappaB level in lung, lung accumulation of neutrophils, and lung microvascular injury were measured. LPS-challenged rats had increased NF-kappaB activity and decreased I-kappaB level in lung, compared to controls. GH dramatically enhanced NF-kappaB activation and I-kappaB degradation induced by LPS challenge. LPS plus GH treatment increased lung accumulation of neutrophils, compared with LPS treatment. Also, subsequently, GH treatment increased lung microvascular injury induced by LPS. These findings suggest that treatment with GH is harmful, instead of beneficial, to LPS-induced organ injury. Increased NF-kappaB activation may be a critical in vivo mechanism that mediates GH action on LPS-induced organ injury. Thus, it is appropriate to rethink GH administration in critical illnesses; further studies are required to evaluate the safety and clinical benefits of GH administration in such conditions.
Ketamine may be advantageous for anesthesia of patients with sepsis caused by gram-negative bacteria, because ketamine may suppress LPS-induced production of proinflammatory cytokines, such as TNFalpha and IL-6. NFkappaB is an important transcription factor that is involved in the post-transcriptional regulation of mRNA expression for several immunoinflammatory mediators in response to endotoxemia. This study examined the effect of ketamine on NFkappaB activation and TNFalpha production in rat peripheral blood mononuclear cells (PBMC). The PBMC were incubated in the presence or absence of LPS and with graded concentrations of ketamine. The culture supernatants and cells were collected for each group and duration of incubation. Activation of NFkappaB was determined by electrophoretic mobility shift assay (EMSA), and the expression of IkappaBalpha, its inhibitor, in PBMC was analysed by Western blotting. TNFalpha levels in the supernatants were measured using a specific enzyme-linked immunosorbent assay (ELISA). LPS stimulation of rat PBMC increased TNFalpha production and NFkappaB activation, with corresponding loss of IkappaBalpha. Ketamine significantly reduced the LPS-induced NFkappaB activation and inhibited TNFalpha production in a dose-dependent manner. These in vitro findings suggest that ketamine is a potent inhibitor of NFkappaB activation and cytokine production in rat PBMC.