Study of three types of desensitizers in dentin bonding strength.

One hundred and twenty human molars without decay (premolars and complete third molars) freshly extracted for orthodontic purposes were used in the study to explore the impact of application of three kinds of desensitizers on self-etching/all-etching bond strength of dentin. The roots were ground along the cementoenamel junction (CEJ), the residual crowns were divided into two parts along mesial and distal direction, and the enamel layer was removed. The dentin was ground into standard pieces of 3x3x3 mm and then polished using alumina waterproof abrasive paper. Two hundred and forty specimens were divided into two groups according to self-etching bond (OptiBond, iBond, XenoIV) and all-etching bond (OptiBond, iBond, Probond). Each of the two groups were subdivided into three groups with different brands, and then further subdivided into three experimental groups and a control group (10 samples in each final group). The surface of dentin coated with desensitizer was examined using scanning electron microscope. Results showed that only the shear strength of iBond + Ddes + Z100 resin group was lower compared to the control group (P < 0.05). The comparison of the resin shear strength in other experimental groups with the control groups demonstrated no statistically significant difference (P > 0.05). The shear strength of Optibond + Gluma, Optibond + Ddes, iBond + Ddes + Z100 resin group in all-etching bond group and the experimental groups in Probond group was lower than in the control group (P < 0.05). The resin shear strength in other groups did not differ from the controls (P > 0.05).

Financial burden on the families of patients with hepatitis B virus-related liver diseases and the role of public health insurance in Yunnan province of China.

OBJECTIVE: To investigate the financial burden of patients who had various stages of hepatitis B virus-related diseases and the level of alleviation from financial burden by health insurance schemes in Yunnan province of China. STUDY DESIGN: A cross-sectional survey. METHODS: Patients' information was consecutively recorded at the First Affiliated Hospital of Kunming Medical University, from December 2012 to June 2013. Consecutive cases of hepatitis B virus (HBV) (520), compensated cirrhosis (91), decompensated cirrhosis (198) and hepatocellular carcinoma (HCC) (131) were recruited from the outpatient and inpatient departments. The total direct costs, hospital charge, outpatient costs, hospitalization fees being reimbursed and household catastrophic health expenditure were estimated for each disease group. RESULTS: The average annual direct costs for each disease group were 19,496 RMB for HBV, 28,466 RMB in compensated cirrhosis, 46,061 RMB for decompensated cirrhosis, and 33,044 RMB for HCC patients. Catastrophic health expenditure occurred in all four groups. Health insurance reimbursement released the financial burden incurred by medical expenses of patients under a high level of household economic status. Public health insurance schemes helped the patients to various extents. CONCLUSIONS: Among these patient groups, direct costs represent a significant economic burden. Health expenditure and financing systems must be considered to prevent the increase of household catastrophe, particularly among the poor.

The relationship between the internal oxidation-reduction system and fetal distress on pregnant patients with intrahepatic cholestasis.

OBJECTIVE: To discuss the relationship between the internal oxidation-reduction system and fetal distress in pregnant patients with intrahepatic cholestasis in order to provide a new basis for clinical treatment and research. PATIENTS AND METHODS: From March 2012 to March 2015, eighty patients with intrahepatic cholestasis of pregnancy (ICP) were selected and divided into two groups: the distressed group (n = 31) and non-distressed group (n = 49). We compared the two groups for differences in MDA, SOD, NO level, GSH level, venous blood and total bile acid level. The relevance of the oxidation-reduction system indicators and the venous blood and total bile acid levels, as well as the differences in the delivery outcome and fetal distress, were compared between the two groups. RESULTS: The serum MDA level of the distressed group was higher than the non-distressed group while the SOD, NO, and GSH levels were lower than the non-distressed group. All differences were statistically significant (p < 0.05). Both the venous blood and total bile acid levels in the distressed group were higher than the non-distressed group and were statistically significant (p < 0.05). Based on Pearson's analysis, MDA was positively associated with the venous blood and total bile acid levels while SOD, NO and GSH levels were negatively associated with it. All differences were statistically significant (p < 0.05). The death rate of cesarean section and perinatal infant in the distressed group were higher than that of the non-distressed group. The proportion of mild and severe asphyxia was higher than the non-distressed group. However, the neonatal weight of the distressed group was lower. All differences were statistically significant (p < 0.05). CONCLUSIONS: The internal oxidation-reduction system indicators of pregnant patients with intrahepatic cholestasis, which are MDA, SOD, NO and GSH levels, may contribute to the occurrence of fetal distress.

ORP150 protects against hypoxia/ischemia-induced neuronal death.

Oxygen-regulated protein 150 kD (ORP150) is a novel endoplasmic-reticulum-associated chaperone induced by hypoxia/ischemia. Although ORP150 was sparingly upregulated in neurons from human brain undergoing ischemic stress, there was robust induction in astrocytes. Cultured neurons overexpressing ORP150 were resistant to hypoxemic stress, whereas astrocytes with inhibited ORP150 expression were more vulnerable. Mice with targeted neuronal overexpression of ORP150 had smaller strokes compared with controls. Neurons with increased ORP150 demonstrated suppressed caspase-3-like activity and enhanced brain-derived neurotrophic factor (BDNF) under hypoxia signaling. These data indicate that ORP150 is an integral participant in ischemic cytoprotective pathways.

Rapid detection of Salmonella typhimurium in chicken carcass wash water using an immunoelectrochemical method.

An immunoelectrochemical method coupled with immunomagnetic separation was developed for rapid detection of Salmonella Typhimurium in chicken carcass wash water. Samples of chicken carcass wash water were inoculated with Salmonella Typhimurium at different cell numbers. Possible nonspecified inhibitors in the wash water were minimized by filtration and centrifugation. An approximately 9.4% loss of Salmonella cells was found after filtration (P < 0.01). The samples were mixed with anti-Salmonella-coated magnetic beads (ASCMB) and alkaline phosphatase-labeled anti-Salmonella (APLAS) to form ASCMB-Salmonella-APLAS conjugates. The conjugates were separated from the solution using a magnetic separator and then incubated with phenylphosphate substrate to produce phenol. The number of Salmonella was determined by measuring the phenol concentration using an amperometric tyrosinase carbon paste electrode in a flow injection analysis system. Under optimized parameters (1 mM MgCl2, 0.2 microg/ml APLAS, and 1 mM phenylphosphate in pH 7.0 Tris buffer solution), Salmonella Typhimurium in chicken carcass wash water could be identified and enumerated within 2.5 h with a detection limit of 5 x 10(3) CFU/ml. A linear relationship on a log-log scale was found between Salmonella cell number and the peak current ratio for Salmonella concentrations ranging from 10(3) to 10(7) CFU/ml (R2 = 0.963). The peak currents of multibacteria samples, containing Salmonella Typhimurium, Listeria monocytogenes, and Campylobacter jejuni, were not significantly different from Salmonella-only samples (P > 0.01).

The small GTP-binding protein TC10 promotes nerve elongation in neuronal cells, and its expression is induced during nerve regeneration in rats.

We have made a rat cDNA library using nerve-transected hypoglossal nuclei. Using this library, we performed expressed-sequence tag analysis coupled with in situ hybridization to identify genes whose expression is altered in response to nerve injury. In this gene screening, a member of Rho family GTPases, TC10, which had not yet been characterized in neuronal cells, was identified. TC10 mRNA expression was very low in normal motor neurons; however, axotomy induced its expression dramatically. Other family members such as RhoA, Rac1, and Cdc42 were moderately expressed in normal motor neurons and showed slight upregulation after axotomy. The expression level of TC10 mRNA was low in the embryonic brain and gradually increased with development. However, the expression of TC10 mRNA in the adult brain was lower and more restricted than that of RhoA, Rac1, and Cdc42. Cultured dorsal root ganglia exhibited dramatic neurite extension secondary to adenovirus-mediated expression of TC10. It can be concluded that although TC10 expression is lower in developing and mature motor neurons compared with other Rho family members, TC10 expression is induced by nerve injury to play a crucial role in nerve regeneration, particularly neurite elongation, in cooperation with other family members.

Changes in mRNA for post-synaptic density-95 (PSD-95) and carboxy-terminal PDZ ligand of neuronal nitric oxide synthase following facial nerve transection.

When the axon of motoneurons is transected, the number of synaptic boutons contacting the cell body is decreased, and the recovery of synapses depends on muscle reinnervation. Post-synaptic density-95 (PSD-95) is a protein which is located at the post-synaptic density (PSD) and it plays a pivotal role in regulating synaptic plasticity and synaptogenesis. In addition, PSD-95 binds with neuronal nitric oxide synthase (nNOS), which is competitively inhibited by carboxy-terminal PDZ ligand of nNOS (CAPON) and, thereby, nNOS activity is thought to be regulated by PSD-95 and CAPON. We investigated the changes in mRNA for PSD-95, CAPON and nNOS in the facial motor nucleus of adult rats following axotomy, by in situ hybridization, in combination with the time course of muscle reinnervation, by retrograde tracing and nNOS protein expression, by examining nicotinamide adenine nucleotide phosphate diaphorase (NADPH-d) activity. Signals of mRNA for PSD-95 and CAPON were initially expressed in the facial motoneurons, transiently decreased following axotomy and gradually recovered to the control level. When reinnervation of the axotomized nerve into muscle was observed, mRNA expression of PSD-95 and CAPON started to recover in the facial motoneurons. It was also found that mRNA and protein expression of nNOS started to increase in the axotomized facial motoneurons just prior to the recovery of mRNA expression of PSD-95 and CAPON. These results suggest that PSD-95 and CAPON are involved in synaptogenesis and/or recovery of synaptic function in motoneurons after axotomy.

Changes in mRNA of protein inhibitor of neuronal nitric oxide synthase following facial nerve transection.

Protein inhibitor of neuronal nitric oxide synthase (PIN) is reported as the protein inhibiting neuronal nitric oxide synthase (nNOS) activity by preventing dimerization of nNOS. It was also reported that PIN inhibits the activity of all nitric oxide synthase (NOS) isozymes. We examined the effects of facial nerve transection on PIN mRNA and NOS expression by in situ hybridization for PIN mRNA and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) staining. PIN mRNA was initially expressed and transiently increased from 3 to 5 days and returned to the basal level at 7 days after axotomy in the motoneurons of the facial nucleus. NADPH-d-positive motoneurons were found from 7 days post-operation in the facial nucleus. These results suggest that PIN may interact with NOS from 7 days post-operation.

Tumor necrosis factor induces Bcl-2 and Bcl-x expression through NFkappaB activation in primary hippocampal neurons.

Emerging data indicate that tumor necrosis factor (TNF) exerts a neuroprotective effect in response to brain injury. Here we examined the mechanism of TNF in preventing neuronal death in primary hippocampal neurons. TNF protected neurons against hypoxia- or nitric oxide-induced injury, with an increase in the anti-apoptotic proteins Bcl-2 and Bcl-x as determined by Western blot and reverse transcriptase-polymerase chain reaction analysis. Treatment of neurons with an antisense oligonucleotide to bcl-2 mRNA or that to bcl-x mRNA blocked the up-regulation of Bcl-2 or Bcl-x expression, respectively, and partially inhibited the neuroprotective effect induced by TNF. Moreover, adenovirus-mediated overexpression of Bcl-2 significantly inhibited hypoxia- or nitric oxide-induced neuronal death. To examine the possible involvement of a transcription factor, NFkappaB, in the regulation of Bcl-2 and Bcl-x expression in TNF-treated neurons, an adenoviral vector capable of expressing a mutated form of IkappaB was used to infect neurons prior to TNF treatment. Expression of the mutant NFkappaB completely inhibited NFkappaB DNA binding activity and inhibited both TNF-induced up-regulation of Bcl-2 and Bcl-x expression and neuroprotective effect. These findings indicate that induction of Bcl-2 and Bcl-x expression through NFkappaB activation is involved in the neuroprotective action of TNF against hypoxia- or nitric oxide-induced injury.

Treatment for congenital synostosis of the fourth and fifth metacarpals with the hemicallotasis technique.

The hemicallotasis technique was used to treat the fifth metacarpal in a hand with congenital synostosis of the fourth and fifth metacarpals. Lengthening and correction of the metacarpal were achieved simultaneously. Continuous traction eliminated further soft-tissue procedures. The appearance and function of the hand were much improved.