MAC(EI) and MAC(awake) of sevoflurane in infants with obstructive jaundice.

BACKGROUND: The aim of this study was to determine whether the MACEI and MACawake of sevoflurane in infants with obstructive jaundice are different from that observed in nonjaundiced infants. METHODS: Infants scheduled for abdominal surgery were recruited into the study. General anesthesia was induced with 8% sevoflurane inhaled with 8 l·min(-1) of oxygen via mask, followed by adjustment of inspired sevoflurane to the target concentration based on the result in previous patient at which laryngoscopy and tracheal intubation were attempted and maintained for 15 min. All responses to tracheal intubation were assessed. At the end of the procedure, sevoflurane was titrated to the target concentration, which was kept constant for 15 min before a standard stimulus was applied to determine whether the infant was awake. The Dixon's 'up and down' method was used to determine progression of subsequent concentrations. RESULTS: There was no significant difference between the MACEI of sevoflurane in infants with obstructive jaundice (3.40 ± 0.21%) and that observed in the control group (3.43 ± 0.18%). But the MACawake of sevoflurane in jaundiced infants (1.00 ± 0.15%) was significantly lower than that of nonjaundiced controls (1.40 ± 0.21%; P = 0.004); to complement these findings, we reported a negative correlation between serum total bilirubin and the probability of awakening (OR = 0.984, 95% CI is 0.970-0.998, P = 0.028). CONCLUSIONS: The MACawake of sevoflurane was reduced in obstructive jaundiced infants compared with nonjaundiced controls, whereas there was no significant difference between the MACEI of sevoflurane in infants with obstructive jaundice and that observed in nonjaundiced infants.

Translational investigation and treatment of neuropathic pain.

Neuropathic pain develops from a lesion or disease affecting the somatosensory system. Translational investigations of neuropathic pain by using different animal models reveal that peripheral sensitization, spinal and cortical plasticity may play critical roles in neuropathic pain. Furthermore, descending facilitatory or excitatory modulation may also act to enhance chronic pain. Current clinical therapy for neuropathic pain includes the use of pharmacological and nonpharmacological (psychological, physical, and surgical treatment) methods. However, there is substantial need to better medicine for treating neuropathic pain. Future translational researchers and clinicians will greatly facilitate the development of novel drugs for treating chronic pain including neuropathic pain.

Methylation of PTCH1a gene in a subset of gastric cancers.

AIM: To establish if PTCH1a transcriptional regulation region (TRR) is methylated in gastric cancer and its influence in gastric tumorigenesis. METHODS: The CpG islands in PTCH1a TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp (the transcription initiation site of PTCH1a was designated as 0) that contained 19 CpG sites was chosen for bisulfite-sequencing PCR (BSP) and methylation-specific PCR (MSP) detection. The gastric cancer cell line AGS was treated with 5-aza-2'-deoxycytidine (5-Aza-dC; 1 micromol/L) for 3 d. Alterations in PTCH1a TRR methylation in treated AGS cells was measured through BSP clone sequences, and their PTCH1 expression was measured by quantitative RT-PCR. The cell cycle and apoptosis were observed with flow cytometry through propidium iodide (PI) staining or annexin V/PI double staining. The prevalence of PTCH1a TRR methylation was investigated in 170 gastric cancer tissue samples and the adjacent normal tissues by MSP. The correlation of PTCH1a TRR methylation with PTCH1 expression or with patients' clinical features was analyzed. RESULTS: Methylation of PTCH1a TRR was observed in AGS cells and a subset of gastric cancer tissues (32%, 55/170), while no methylation amplification products were observed in any normal tissues by MSP. The methylation of PTCH1a TRR was correlated negatively with PTCH1 expression (Spearman's r = -0.380, P = 0.000). However, methylation of PTCH1a TRR was not related to the gastric cancer patients' clinical features, such as sex, age of onset, clinical stage, lymph node metastasis or histological grade. The methylation of PTCH1a TRR in AGS cells was almost converted to non-methylation after 5-Aza-dC treatment, which increased PTCH1 expression (5.3 +/- 2.5 times; n = 3) and apoptosis rate (3.0 +/- 0.26 times; P < 0.05; n = 3). CONCLUSION: Methylation of PTCH1a TRR is present in a subset of gastric cancers and correlated negatively with PTCH1 expression. This may be an early event in gastric tumorigenesis and a new treatment target.