Effect of low-pressure pneumoperitoneum on pain and inflammation in laparoscopic cholecystectomy: a randomized controlled clinical trial.

OBJECTIVE: We aim to assess the effect of low-pressure pneumoperitoneum on post operative pain and ten of the known inflammatory markers. BACKGROUND: The standard of care pneumoperitoneum set pressure in laparoscopic cholecystectomy is set to 12-14 mmHg, but many societies advocate to operate at the lowest pressure allowing adequate exposure of the operative field. Many trials have described the benefits of operating at a low-pressure pneumoperitoneum in terms of lower post operative pain, and better hemodynamic stability. But only few describe the effects on inflammatory markers and cytokines. METHODS: A prospective, double-blinded, randomised, controlled clinical trial, including patients who underwent elective laparoscopic cholecystectomy. Patients randomised into low-pressure (8-10 mmHg) vs. standard-pressure (12-14 mmHg) with an allocation ratio of 1:1. Perioperative variables were collected and analysed. RESULTS: one hundred patients were allocated, 50 patients in each study arm. Low-pressure patients reported lower median pain score 6-hour post operatively (5 vs. 6, p-value = 0.021) in comparison with standard-pressure group. Eight out of 10 inflammatory markers demonstrated better results in low-pressure group in comparison with standard-pressure, but the effect was not statistically significant. Total operative time and surgery difficulty was not significantly different between the two groups even in the hands of inexperienced surgeons. CONCLUSION: low-pressure laparoscopic cholecystectomy is associated with less post operative pain and lower rise of inflammatory markers. It is feasible with comparable complications to the standard of care. Registered on ClinicalTrials.gov (NCT05530564/ September 7th, 2022).

An analysis on the expression level and influencing factors of CD4 +CD25 + regulatory cells among male drug -abusers with syphilis / 预防医学

Objective To explore the expression level and influencing factors of CD4 +CD25 + regulatory cells(Treg)among male drug -abusers with syphilis.Methods 144 male drug -abusers with syphilis,41 male drug -abusers without syphilis,35 male non -drug abuser with syphilis and 35 male healthy volunteers were enrolled in this study.Expression levels of CD4 +CD25 +Treg of them were detected.A questionnaire interview was conducted among these participants, including drug abuse duration,drug types and abuse ways.Results The levels of Treg expression of drug -abusers with syphilis were significantly higher than that of drug -abusers without syphilis and non -drug abuser with syphilis (P <0.01 ).Despite of the stage of syphilis,types of drugs and abuse way,Treg expression levels with drug abuse duration of"above 1 -year"were significantly higher than those of "1 -year or below"(P <0.01 ).Treg expression levels were positively correlated to drug abuse duration (R2 =0.672,P <0.01)among patients.Among the participants,people both with traditional and new drugs were significantly higher than that with only traditional or new drug (P <0.01).In addition, people both with injecting and non -injecting abuse were significantly higher than that with one way of drug -abuse (P <0.01).Among those with drug abuse duration of "above 1 -year",Treg levels of drug -abusers with traditional drugs and injecting abuse way were remarkably higher than that with new drug and non -injecting abuse respectively (P <0.01). Conclusion Among male drug -abusers with syphilis,suppression of cellular immune function resulting from increased CD4 +CD25 +regulatory T cells is related to drug abuse duration,and is also influenced by drug types and abuse ways.

Effects of hypothermia on NSE and S-100 protein levels in CSF in neonates following hypoxic/ischaemic brain damage.

AIM: The aim of the study was to evaluate the effects of hypothermia on neuron-specific enolase (NSE) and S-100 protein levels in cerebrospinal fluid (CSF) in neonates with hypoxic/ischaemic encephalopathy (HIE). METHODS: Fifty-one enrolled neonates with HIE were divided into two groups: hypothermia (n = 23) and control (n = 28). NSE and S-100 protein were measured with immunoradiometric assays. Amino acid neurotransmitters were also measured by reversed-phase high-performance liquid chromatography. Neurodevelopmental assessments were performed at 3 and 12 months of age. RESULTS: Neuron-specific enolase and S-100 levels were lower, and neurodevelopment outcome was better in the hypothermia group compared with the control group. Among the infants who received hypothermia, CSF NSE and S-100 were significantly higher in those who developed severe neurological impairment (mental development index or physical development index <70). There were no significant differences between the two groups in amino acid neurotransmitters. CONCLUSION: These results indicated that hypothermia was associated with decreased CSF NSE and S-100 level and correlated with neurodevelopmental outcome in infants with HIE.

VEGF-mediated angiogenesis stimulates neural stem cell proliferation and differentiation in the premature brain.

This study investigated the effects of angiogenesis on the proliferation and differentiation of neural stem cells in the premature brain. We observed the changes in neurogenesis that followed the stimulation and inhibition of angiogenesis by altering vascular endothelial growth factor (VEGF) expression in a 3-day-old rat model. VEGF expression was overexpressed by adenovirus transfection and down-regulated by siRNA interference. Using immunofluorescence assays, Western blot analysis, and real-time PCR methods, we observed angiogenesis and the proliferation and differentiation of neural stem cells. Immunofluorescence assays showed that the number of vWF-positive areas peaked at day 7, and they were highest in the VEGF up-regulation group and lowest in the VEGF down-regulation group at every time point. The number of neural stem cells, neurons, astrocytes, and oligodendrocytes in the subventricular zone gradually increased over time in the VEGF up-regulation group. Among the three groups, the number of these cells was highest in the VEGF up-regulation group and lowest in the VEGF down-regulation group at the same time point. Western blot analysis and real-time PCR confirmed these results. These data suggest that angiogenesis may stimulate the proliferation of neural stem cells and differentiation into neurons, astrocytes, and oligodendrocytes in the premature brain.

Ischemia induced neural stem cell proliferation and differentiation in neonatal rat involved vascular endothelial growth factor and transforming growth factor-beta pathways.

Brain ischemia is a leading cause of mortality and morbidity in premature infants. Knowing the fate of neural stem cells in the subventricular zone (SVZ) after ischemia and the mechanisms that determine this fate would be useful in manipulating neural stem cell proliferation and differentiation and possibly in reversing ischemic damage. We sought to identify the genes involved in the proliferation and differentiation of neural stem cells after exposure to ischemia in a 3-day-old rat model that approximates ischemia in premature infants. Proliferating cells were labeled by bromodeoxyuridine (BrdU) through intraperitoneal injection. Using immunfluorescence assays, we observed the proliferation and differentiation of neural stem cells. Genes were identified with GeneChip and real-time quantitative polymerase chain reaction analysis. Ischemic rats had more BrdU-positive cells in the SVZ at all four time points and more neural stem cells differentiation into neurons, astrocytes, and oligodendrocytes. GeneChip analysis showed a 3- to 10-fold increase in the mRNA expression of vascular endothelial growth factor, transforming growth factor-beta, and their receptors in the SVZ. PCR assays and Western blot analyses confirmed these results, indicating that vascular endothelial growth factor and transforming growth factor-beta might be two of the factors that involve post-ischemic neural stem cell proliferation and differentiation.

H2O2/HCl and heat-treated Ti-6Al-4V stimulates pre-osteoblast proliferation and differentiation.

The purpose of the present study was to evaluate the bioactivity of chemical treatment of titanium alloy (Ti-6Al-4V) in vitro. Smooth-surface discs of Ti-6Al-4V were used in this study. Sandblasted, dual acid-etched and H(2)O(2)/HCl heat-treated discs were set as test group, and sandblasted, dual acid-etched discs as control group. SEM and XRD analysis revealed a porous anatase gel layer on rough surface in the test group and a rough surface in the control group. Mouse pre-osteoblasts (MC3T3-E1 cells) were cultured on these 2 group discs, and then cell proliferation and differentiation were examined 4 days, 7 days, and 14 days after cell seeding. Cell proliferation was greatly stimulated at all time points when cultured in test group (P < .05). The alkaline phosphatase (ALP) activity and osteocalcin (OC) production were much higher in the test group compared with the control group at every time point investigated (P < .05). Furthermore, in the test group, the expressions of alkaline phosphatase-2, osteocalcin, and collagen type I alpha 1 mRNAs were significantly up-regulated as compared with those in the control group (P < .05 or P < .01). The results suggested that H(2)O(2)/HCl and heat-treatment might facilitate better integration of Ti-6Al-4V implants with bone.

[Neurogenesis in the subventricular zone of neonatal rats after ischemic brain injury].

OBJECTIVE: To study the proliferation and differentiation of neural stem cells in the subventricular zone (SVZ) in neonatal rats after bilateral common arteries occlusion. METHODS: Ninety-six 3-day-old Sparuge-Dawley rats were randomly divided into two groups: ischemia and control. Rats in the ischemia group were subjected to bilateral common arteries occlusion and the rats in the control group were sham-operated. All rats were administrated with 5-bromodeoxyuridine (BrdU) (50 mg/kg) via intraperitoneal injection. Rats were sacrificed and their brains were removed 1, 4, 7, 10, 14 and 35 days after ischemia. Using brain paraffin sections and immunofluorescence assays, the number of newborn cells in the SVZ was counted. Newborn neural stem cells and oligodendrocytes in the SVZ were observed, and then double marked with BrdU and nestin or osmium tetroxide (O4). RESULTS: The number of BrdU+ cells (neural stem cells) in the SVZ in the ischemia group was greater than in the control group 4, 7, 10 and 14 days after ischemia, and reached a peak at 4 days after ischemia (253.1+/- 49.3 vs 133.5+/- 17.7; P< 0.01). By 35 days after ischemia, the number of BrdU+/O4+ cells (oligodendrocytes) in the corpus callosum (56.0+/- 7.2 vs 17.0+/- 6.4; P< 0.01), the septal nuclei (45.0+/- 11.9 vs 20.5+/- 5.0; P< 0.01), the striatum (34.5+/- 4.2 vs 14.5+/- 5.8; P< 0.01) and the olfactory bulb (46.5+/- 6.6 vs 23.5+/- 8.4; P< 0.01) in the ischemia group increased significantly as compared to the control group (P< 0.01). CONCLUSIONS: Brain ischemia can activate the proliferation of neural stem cells in the SVZ and promote neural stem cells differentiation into oligodendrocytes. The immature brain may have the capacity for self-repair after ischemic brain injury.