[Experimental study on evaluating renal redox metabolism in renal ischemia-reperfusion injury using GluCEST imaging with 3.0 T MRI].

Objective: To investigate the feasibility of 3.0 T glutamate chemical exchange saturation transfer (GluCEST) imaging in evaluating renal redox metabolism in renal ischemia-reperfusion injury (IRI). Methods: Rabbits in the IRI group (n=56) underwent surgery by clamping the left renal artery for 45 min and then releasing to establish IRI. Rabbits in the sham group (n=8) underwent the same operation without clamping the left renal artery. GluCEST MRI was performed before and at 1 h, 12 h, 1 day, 3 days, 7 days, and 14 days after the operations, with eight rabbits in the IRI group sacrificed immediately after each scanning and eight in the sham group sacrificed at 14 days after scanning. The left kidneys were removed for histopathological examination and reactive oxygen species (ROS) fluorescence staining. Differences in the magnetic resonance ratio asymmetry (MTRasym) of the renal cortex and outer medulla among different groups were compared. Correlations between the MTRasym and ROS were analyzed. Results: The MTRasym of the renal cortex in the sham and IRI subgroups were higher than that of the outer medulla (t=8.16, P<0.001; t=4.78, P=0.002; t=4.94, P=0.002; t=5.76, P=0.001, t=6.68, P<0.001; t=6.40, P<0.001; t=5.16, P=0.001; t=3.30, P=0.013). The MTRasym of the renal cortex and outer medulla in the IRI-1h, IRI-12h, IRI-1d, IRI-3d, IRI-7d, and IRI-14d groups were lower than in the sham and IRI-pre groups (all P<0.05). The MTRasym of the renal cortex and outer medulla in the IRI-1h group were lower than in the IRI-12h, IRI-1d, IRI-3d, IRI-7d, and IRI-14d groups (all P<0.05). The MTRasym of the renal cortex in the IRI-12h group was lower than in the IRI-7d and IRI-14d groups (1.84%±0.09% vs.2.42%±0.19%, 2.41%±0.31%, all P<0.05). The MTRasym of the renal cortex in the IRI-1d group was lower than in the IRI-7d group (1.99%±0.17% vs. 2.42%±0.19%, P=0.008). The MTRasym of the outer medulla in the IRI-12h group was lower than in the IRI-3d, IRI-7d, and IRI-14d groups (1.32%±0.27% vs. 1.79%±0.31%, 1.98%±0.18%, 1.66%±0.40%, respectively, all P<0.05]. The MTRasym of the outer medulla in the IRI-7d group was higher than in the IRI-1d and IRI-14d groups (1.98%±0.18% vs. 1.52%±0.31%, 1.66%±0.40%, all P<0.05). The MTRasym of the renal cortex and outer medulla had a strong negative correlation with the mean fluorescence intensity of ROS (ρ=-0.889, P<0.001; ρ=-0.784, P<0.001). Conclusion: 3.0 T GluCEST imaging can indirectly reflect the changes of renal redox metabolism in renal IRI.

[Activation of GABAergic neurons in the zona incerta accelerates anesthesia induction with sevoflurane and propofol without affecting anesthesia maintenance or awakening in mice].

OBJECTIVE: To explore the regulatory effects of GABAergic neurons in the zona incerta (ZI) on sevoflurane and propofol anesthesia. METHODS: Forty-eight male C57BL/6J mice divided into 8 groups (n=6) were used in this study. In the study of sevoflurane anesthesia, chemogenetic experiment was performed in 2 groups of mice with injection of either adeno-associated virus carrying hM3Dq (hM3Dq group) or a virus carrying only mCherry (mCherry group). The optogenetic experiment was performed in another two groups of mice injected with an adeno-associated virus carrying ChR2 (ChR2 group) or GFP only (GFP group). The same experiments were also performed in mice for studying propofol anesthesia. Chemogenetics or optogenetics were used to induce the activation of GABAergic neurons in the ZI, and their regulatory effects on anesthesia induction and arousal with sevoflurane and propofol were observed; EEG monitoring was used to observe the changes in sevoflurane anesthesia maintenance after activation of the GABAergic neurons. RESULTS: In sevoflurane anesthesia, the induction time of anesthesia was significantly shorter in hM3Dq group than in mCherry group (P < 0.05), and also shorter in ChR2 group than in GFP group (P < 0.01), but no significant difference was found in the awakening time between the two groups in either chemogenetic or optogenetic tests. Similar results were observed in chemogenetic and optogenetic experiments with propofol (P < 0.05 or 0.01). Photogenetic activation of the GABAergic neurons in the ZI did not cause significant changes in EEG spectrum during sevoflurane anesthesia maintenance. CONCLUSION: Activation of the GABAergic neurons in the ZI promotes anesthesia induction of sevoflurane and propofol but does not affect anesthesia maintenance or awakening.

Prognostic significance of CD163 expression and its correlation with cyclooxygenase-2 and vascular endothelial growth factor expression in cutaneous melanoma.

In several cancers, tumor progression is associated with the infiltration of tumor-associated macrophages (TAMs). The aim was to evaluate the prognostic significance of expression of CD163 and CD68 (TAMs' markers) and their correlation with vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2) expression in cutaneous melanoma. Diagnostic tissues from 102 patients of cutaneous melanoma were evaluated by immunohistochemistry for their CD68, CD163, VEGF, and COX-2 expression. Correlations between the proteins were then investigated. Clinicopathological features, overall survival (OS), and progression-free survival were analyzed in terms of the expression of these proteins. CD163, but not CD68, expression correlated with VEGF and COX-2 expression. High expression for CD163 was associated with a deeper Breslow thickness and an advanced stage of the disease. High expression of CD163 was associated with lower OS. No significant differences were noted in CD68 expression between the clinicopathological variables and the OS. COX-2 expression was associated with a deeper Breslow thickness and a higher frequency of lymph node involvement. Multivariate analysis revealed that CD163 expression and COX-2 expression were independent prognostic markers of lower survival outcomes. Our data confirmed that CD163 expression provides independent prognostic information in cutaneous melanoma. The correlation of CD163 with VEGF and COX-2 expression suggests various tumor-promoting actions of CD163-positive TAMs.

Clinicopathological significance of tumor-infiltrating lymphocytes and programmed death-1 expression in cutaneous melanoma: a comparative study on clinical subtypes.

Interactions between immune cells and tumor cells play an important role in tumor progression. We evaluated patterns of tumor-infiltrating lymphocytes (TILs) and programmed death-1 (PD-1) expression in acral and nonacral cutaneous melanoma, and determined their effects on clinicopathological characteristics and biologic responses. We identified 122 cases of cutaneous melanoma, of which 39 were cases of non-nail unit acral melanoma (NNUAM), 35 were cases of nail unit melanoma (NUM), and 48 were cases of nonacral melanoma. Clinicopathological features and survival outcomes were analyzed according to the scores for TILs and PD-1 expression in intratumoral and peritumoral compartments. The effects of the presence of TILs and PD-1 expression on various clinicopathological factors differed according to the clinical subtypes of cutaneous melanoma. The frequency of intratumoral TILs and PD-1 expression were lower in NUM than in the other two subtypes. The density of peritumoral PD-1 was significantly higher in NNUAM. In NUM and nonacral melanoma, a low density of intratumoral TILs and PD-1 was associated with a deeper Breslow thickness and the presence of a vertical growth phase. In NNUAM, a high density of peritumoral TILs and PD-1 was associated with a shallower Breslow thickness and less frequent extracutaneous dissemination. In NNUAM, a high density of peritumoral PD-1 was associated with a better prognosis. This study suggests that the effects of PD-1+ TILs on biological activity differ according to the clinical subtypes of cutaneous melanoma.

[Role and mechanism of hydrogen sulfide in cigarette smoke induced chronic obstructive pulmonary disease related pulmonary vascular remodeling in rats].

Objective: To investigate the role and mechanism of hydrogen sulfide (H2S) in rats with chronic obstructive pulmonary disease (COPD) related pulmonary vascular remodeling. Methods: Twenty four healthy male Sprague-Dawley rats were randomly divided into 4 groups: control group, cigarette smoke (CS) group, CS+ Sodium hydrosulfide (NaHS) group and CS+ DL-propargylglycine (PPG) group. Rats in control group were fed normally and breathed clear air, and for the rest groups, passive cigarette smoke inhalation method were adopted to establish COPD model. After 8 weeks, the rats in corresponding groups were treated by NaHS or PPG. After 16 weeks, the markers of pulmonary vascular remodeling in all groups were measured. Proliferation marker proliferative cell nuclear antigen (PCNA) and oxidative stress marker 3-neurotrophin (3-NT) in all groups were measured by immunohistochemistry (IHC). Results: Compared with control group, the airway resistance was increased (0.859±0.283 vs 0.578±0.088, P<0.05) and the pathological scores was much higher in CS group, which suggested that the COPD model was successful. The degree of small resistance pulmonary artery medial wall thickness and full vascular muscularization of CS group were much higher (0.54±0.20 vs 0.37±0.12, 0.39±0.08; 0.61±0.16 vs 0.20±0.12, 0.34±0.13, all P<0.01)than control group and CS+ NaHS group, there was no significant difference between CS+ PPG group and CS group. In accordance with the results of morphometric analysis, the proliferation marker PCNA was more in CS group when compared with control group and CS+ NaHS group (0.27±0.08 vs 0.12±0.06, 0.14±0.06, both P<0.05), there was no significant difference between CS+ PPG group and CS group. Furthermore, the IHC also showed that 3-NT significantly increased in CS group compared with control group and CS+ NaHS group (0.26±0.08 vs 0.18±0.04, 0.19±0.06, both P<0.01), there was no significant difference between CS+ PPG group and CS group as well. In addition, the small resistance pulmonary artery medial wall thickness had strong correlation with the expression level of oxidative stress marker 3-NT (r=0.906, P<0.001). Conclusion: H2S significantly attenuates cigarette smoke induced COPD related pulmonary vascular remodeling, which could be related to its ability to decrease oxidative stress.

The effect of surgical and psychological stress on learning and memory function in aged C57BL/6 mice.

Postoperative cognitive dysfunction (POCD) is an important complication following major surgery and general anesthesia in older patients. However, the etiology of POCD remains largely to be determined. It is unknown how surgical stress and psychological stress affect the postoperative learning and memory function in geriatric patients. We therefore established a pre-clinical model in aged C57BL/6 mice and aimed to investigate the effects of surgical stress and psychological stress on learning and memory function and the possible roles of the protein kinase B/mammalian target of rapamycin (AKT/mTOR) pathway. The surgical stress was induced by abdominal surgery under local anesthesia, and the psychological stress was induced by a communication box. Cognitive functions and markers of the AKT/mTOR pathway were assessed at 1, 3 and 7 days following the stress. The impairments of learning and memory function existed for up to 7 days following surgical stress and surgical stress plus psychological stress, whereas the psychological stress did not affect the cognitive function alone or combined with surgical stress. Analysis of brain tissue revealed a significant involvement of the AKT/mTOR pathway in the impairment of cognition. These data suggested that surgical stress could induce cognitive impairment in aged mice and perioperative psychological stress is not a constitutive factor of POCD. The AKT/mTOR pathway is likely involved as one of the underlying mechanisms of the development of POCD.

Scaling of anomalous Hall effects in facing-target reactively sputtered Fe4N films.

The anomalous Hall effect (AHE) in the reactively sputtered epitaxial and polycrystalline γ'-Fe4N films is investigated systematically. The Hall resistivity is positive over the entire temperature range. The magnetization, carrier density and grain boundary scattering have a major impact on the AHE scaling law. The scaling exponent γ in the conventional scaling of ρAH ∝ ρ(γ)(xx) is larger than 2 in both the epitaxial and polycrystalline γ'-Fe4N films. Although γ > 2 has been found in heterogeneous systems due to the effects of the surface and interface scattering on AHE, γ > 2 is not expected in homogenous epitaxial systems. We demonstrated that γ > 2 results from residual resistivity (ρxx0) in γ'-Fe4N films. Furthermore, the side-jump and intrinsic mechanisms are dominant in both epitaxial and polycrystalline samples according to the proper scaling relation.

Geranylgeranylation signals to the Hippo pathway for breast cancer cell proliferation and migration.

Protein geranylgeranylation (GGylation) is an important biochemical process for many cellular signaling molecules. Previous studies have shown that GGylation is essential for cell survival in many types of cancer. However, the molecular mechanism mediating the cell survival effect remains elusive. In this report, we show that the Hippo pathway mediates GGylation-dependent cell proliferation and migration in breast cancer cells. Blockade of GGylation enhanced phosphorylation of Mst1/2 and Lats1, and inhibited YAP and TAZ activity and the Hippo-YAP/TAZ pathway-dependent transcription. The effect of GGylation blockade on inhibition of breast cancer cell proliferation and migration is dependent on the Hippo-YAP/TAZ signaling, in which YAP appears to regulate cell proliferation and TAZ to regulate cell migration. Furthermore, GGylation-dependent cell proliferation is correlated with the activity of YAP/TAZ in breast cancer cells. Finally, Gγ and RhoA are the GGylated proteins that may transduce GGylation signals to the Hippo-YAP/TAZ pathway. Taken together, our studies have demonstrated that the Hippo-YAP/TAZ pathway is essential for GGylation-dependent cancer cell proliferation and migration.

Recovery of gastrointestinal function with thoracic epidural vs. systemic analgesia following gastrointestinal surgery.

The objective of this review was to systematically assess the effect of thoracic epidural analgesia (TEA) vs. systemic analgesia (SA) on the recovery of gastrointestinal (GI) function in patients following GI surgery. We performed a comprehensive literature search to identify randomized controlled trials of adult patients undergoing GI surgery, comparing the effect of two postoperative analgesia regimens. Patients postoperatively receiving local anesthesia-based TEA with or without opioids were compared to patients receiving opioid-based SA. The outcomes considered were times to GI function recovery, GI complications, and specific side effects. Twelve studies with 331 patients in the TEA group and 319 in the SA group were included. Compared to SA, TEA improved the GI recovery after GI procedures by shortening the time to first passage of flatus by 31.3 h, 95% confidence intervals (CIs): -33.2 to -29.4, P < 0.01; and shortening the time to first passage of stool by 24.1 h, 95% CIs: -27.2 to -20.9, P < 0.001. There was no difference between the groups in the incidence of anastomotic leakage and ileus. The occurrence of postoperative hypotension was relatively higher in the TEA group, risk ratio: 7.9, 95% CIs: 2.4 to 26.5, P = 0.001; other side effects (such as pruritus and vomiting) were similar in the two groups. There is evidence that TEA (compared to SA) improves the recovery of GI function after GI procedures without any increased risk of GI complications. To further confirm these effects, larger, better quality randomized controlled trials with standard outcome measurements are needed.

Aspirin-triggered Lipoxin A4 attenuates mechanical allodynia in association with inhibiting spinal JAK2/STAT3 signaling in neuropathic pain in rats.

Aspirin-triggered Lipoxin A4 (ATL), as a Lipoxin A4 (LXA4) epimer, is endogenously produced by aspirin-acetylated cycloxygenase-2 (COX-2) and plays a vital role in endogenous anti-inflammation via the LXA4 receptor (ALX). Recent investigations have indicated that spinal neuroinflammation and the activation of the Janus Kinase 2 (JAK2)/Signal Transducers and Transcription Activators 3 (STAT3) signaling pathway are involved in neuropathic pain states. However, the effect of ATL on neuroinflammation and JAK2/STAT3 signaling in chronic constriction injury (CCI)-induced neuropathic pain in rats has not been well-studied. The present study demonstrated the anti-inflammatory and analgesic effect of ATL on neuropathic pain and assessed the role of spinal JAK2/STAT3 signaling on the effect of ATL. Intrathecal administration of ATL significantly attenuated mechanical allodynia via spinal ALX and inhibited the upregulation of pro-inflammatory cytokines (IL-1ß, IL-6, and TNF-α) on day 7 of CCI surgery. In addition, ATL markedly suppressed the upregulation of p-STAT3 induced by the neuropathic pain. Blockade of JAK2-STAT3 signaling with intrathecal administration of the JAK2 inhibitor AG490 or the STAT3 inhibitor S3I-201 clearly reduced mechanical allodynia and the upregulation of pro-inflammatory cytokines in CCI rats. Interestingly, inhibition of JAK2/STAT3 signaling via ATL or the specific signaling inhibitor (AG49, S3I-201) further promoted the increased expression of suppressor of cytokine signaling 3 (SOCS3) mRNA in the spinal cord induced by CCI surgery. Taken together, our results suggested that the analgesic effect of ATL was mediated by inhibiting spinal JAK2/STAT3 signaling and hence the spinal neuroinflammation in CCI rats.

Isoflurane unveils a critical role of glutamate transporter type 3 in regulating hippocampal GluR1 trafficking and context-related learning and memory in mice.

Glutamate transporter type 3 (EAAT3) may play a role in cognition. Isoflurane enhances EAAT3 trafficking to the plasma membrane. Thus, we used isoflurane to determine how EAAT3 might regulate learning and memory and the trafficking of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, such as GluR1, to the plasma membrane, a fundamental biochemical process for learning and memory. Here, isoflurane increased EAAT3 but did not change GluR1 levels in the plasma membrane of wild-type mouse hippocampus. Isoflurane increased protein phosphatase activity in the wild-type and EAAT3(-/-) mouse hippocampus. Also, isoflurane reduced GluR1 in the plasma membrane and decreased phospho-GluR1 in EAAT3(-/-) mice. The phosphatase inhibitor okadaic acid attenuated these effects. Finally, isoflurane inhibited context-related fear conditioning in EAAT3(-/-) mice but not in wild-type mice. Thus, isoflurane may increase GluR1 trafficking to the plasma membrane via EAAT3 and inhibit GluR1 trafficking via protein phosphatase. Lack of EAAT3 effects leads to decreased GluR1 trafficking and impaired cognition after isoflurane exposure in EAAT3(-/-) mice.

Involvement of the spinal NALP1 inflammasome in neuropathic pain and aspirin-triggered-15-epi-lipoxin A4 induced analgesia.

Neuroinflammation plays an important role in nerve-injury-induced neuropathic pain, but the explicit molecular mechanisms of neuroinflammation in neuropathic pain remain unclear. As one of the most critical inflammatory cytokines, interleukin-1ß (IL-1ß) has been regarded as broadly involved in the pathology of neuropathic pain. The inflammasome caspase-1 platform is one primary mechanism responsible for the maturation of IL-1ß. Lipoxins, a type of endogenous anti-inflammatory lipid, have proved to be effective in relieving neuropathic pain behaviors. The present study was designed to examine whether the inflammasome caspase-1 IL-1ß platform is involved in chronic constriction injury (CCI)-induced neuropathic pain and in lipoxin-induced analgesia. After rats were subjected to the CCI surgery, mature IL-1ß was significantly increased in the ipsilateral spinal cord, and the inflammasome platform consisting of NALP1 (NAcht leucine-rich-repeat protein 1), caspase-1 and ASC (apoptosis-associated speck-like protein containing a caspase-activating recruitment domain) was also activated in spinal astrocytes and neurons, especially at the superficial laminae of the spinal dorsal horn; The aspirin-triggered-15-epi-lipoxin A4 (ATL), which shares the potent actions of the endogenous lipoxins, was administered to the CCI rats. Repeated intrathecal injection with ATL markedly attenuated the CCI-induced thermal hyperalgesia and significantly inhibited NALP1 inflammasome activation, caspase-1 cleavage, and IL-1ß maturation. These results suggested that spinal NALP1 inflammasome was involved in the CCI-induced neuropathic pain and that the analgesic effect of ATL was associated with suppressing NALP1 inflammasome activation.

Spinal interleukin-33 and its receptor ST2 contribute to bone cancer-induced pain in mice.

Cancer pain, particularly bone cancer pain, affects the quality of life of cancer patients, and current treatments are limited. Interleukin (IL)-33, a new member of the IL-1 super family, has been reported to be involved in the modulation of inflammatory pain. However, studies focused on its role in the modulation of cancer pain have been rare. The present study was designed to investigate whether spinal IL-33/ST2 signaling was involved in bone cancer-induced pain in mice. Bone cancer was induced via intra-femoral inoculation of 4T1 mammary carcinoma cells. The mice inoculated with carcinoma cells showed mechanical allodynia, heat hyperalgesia and a reduction in limb use, whereas phosphate-buffered saline or heat-killed cells-injected mice showed no significant difference compared to non-treated mice. The pain hypersensitive behaviors worsened over time and with bone destruction. Both the mRNA and the protein levels of IL-33 and relative cytokines (IL-1ß, IL-6, TNF-a) were significantly increased in the spinal cord after the inoculation of carcinoma cells. Intrathecal administration of ST2 antibody to block IL-33/ST2 signaling alleviated pain behaviors in a dose-dependent manner in bone cancer pain mice compared with vehicle-injected mice. Moreover, the ST2(-/-) mice showed a significant amelioration of limb use and heat hyperalgesia compared to wild-type mice. Meanwhile, concentrations of spinal IL-1ß, IL-6 and TNF-a in the cancer-bearing ST2(-/-) mice had no significant changes. These data further suggested that IL-33/ST2 signaling played a vital role in cancer pain. Our results provided evidence that IL-33 and its receptor ST2 may be a potential therapeutic target for the treatment of pain in bone cancer patients.

Interleukin-33 mediates formalin-induced inflammatory pain in mice.

Interleukin-33 (IL-33), a member of the IL-1 family, has attracted growing interest since its discovery in 2003. IL-33 has been implicated in many diseases, including arthritis, asthma, allergies, and cardiovascular and infectious diseases. However, few studies have investigated its role in the transmission and modulation of pain. The present study was designed to explore the possible roles of IL-33 and its receptor, ST2, in formalin-induced inflammatory pain in mice. We found that both subcutaneous (s.c., 300 ng) and intrathecal injection (i.t., 3 ng) of recombinant IL-33 (rIL-33) increased paw lifting and licking time not only in normal mice but also in formalin models. Administration of ST2 antibody, which blocked the IL-33/ST2 signaling, alleviated the formalin-induced spontaneous pain behavior. Moreover, the ST2(-/-) mice showed significantly decreased pain behavior, as well as reduced ultrasonic vocalization induced by formalin, compared with the wild-type group. Additionally, ST2 antibody alleviated the potentiating effects of rIL-33 on pain behavior in the formalin mice, indicating that IL-33 plays a role in pain modulation through its ST2 receptor. These data suggest IL-33 and its ST2 receptor mediate formalin-induced inflammatory pain, and as a result this cytokine and its receptor may be new targets for the development of analgesics.

Coexistence of congenital giant melanocytic nevus of the scalp with cranial defect, poliosis, and hair loss.

Congenital melanocytic nevi (CMN) are pigmented lesions presenting on the skin in approximately 1% of all newborns at or shortly after birth. CMN have been described as being associated with several anomalies, including cranial bone hypertrophy, scoliosis, and spina bifida. This is the first report to describe a giant congenital melanocytic nevus on the scalp associated with cranial involvement, poliosis, and alopecia.

Extracellular signal-regulated kinase activation in spinal astrocytes and microglia contributes to cancer-induced bone pain in rats.

Cancer pain, especially cancer-induced bone pain, affects the quality of life of cancer patients, and current treatments for this pain are limited. The present study demonstrates that spinal extracellular signal-regulated kinase (ERK) activation in glial cells plays a crucial role in cancer-induced bone pain. From day 4 to day 21 after the intra-tibia inoculation with Walker 256 mammary gland carcinoma cells, significant mechanical allodynia was observed as indicated by the decrease of mechanical withdrawal thresholds in the von Frey hair test. Intra-tibia inoculation with carcinoma cells induced a vast and persistent (>21 D) activation of ERK in the bilateral L2-L3 and L4-L5 spinal dorsal horn. The increased pERK1/2-immunoreactivity was observed in both Iba-1-expressing microglia and GFAP-expressing astrocytes but not in NeuN-expressing neurons. A single intrathecal injection of the selective MEK (ERK kinase) inhibitors PD98059 (10 µg) on day 12 and U0126 (1.25 and 3 µg) on day 14, attenuated the bilateral mechanical allodynia in the von Frey hair test. Altogether, our results suggest that ERK activation in spinal microglia and astrocytes is correlated with the onset of allodynia and is important for allodynia maintenance in the cancer pain model. This study indicated that inhibition of the ERK pathway may provide a new therapy for cancer-induced bone pain.

Stroke volume variation and pleth variability index to predict fluid responsiveness during resection of primary retroperitoneal tumors in Hans Chinese.

Respiration variation in arterial pulse pressure (ΔPP) and pulse oximetry plethysmographic waveform amplitude (ΔPOP) are accurate predictors of fluid responsiveness in mechanically ventilated patients. We hypothesized that stroke volume variation (SVV) and pleth variability index (PVI) can predict fluid responsiveness in mechanically ventilated patients during major surgical procedures in Hans Chinese. This prospective study consisted of fifty-five Hans Chinese patients undergoing resection of primary retroperitoneal tumors (PRPT). During the surgical procedures, hemodynamic data [central venous pressure (CVP), cardiac index (CI), stroke volume index (SVI), SVV, and PVI] were recorded before and after volume expansion (VE) (8 ml•kg-1 of 6% hydroxyethyl starch 130/0.4). Fluid responsiveness was defined as an increase in SVI ≥ 10% after VE. Four patients were excluded from analysis for arrhythmia or obvious hemorrhage during VE. Baseline SVV correlated well with baseline PVI and the changes in SVV was correlated with the changes in PVI (p < 0.01) after VE. There were significant increases of CI, SVI and decreases of SVV, PVI in responder (Rs) after VE. ROC results showed that the areas for SVV, PVI were significantly higher than the areas for CI, MAP, CVP, PI (p < 0.05). The best threshold values to predict fluid responsiveness were more than 12.5% for SVV and more than 13.5% for PVI in the real surgical setting. The baseline value of SVV, and PVI correlated significantly with volume-induced changes in SVI (p < 0.01). Both SVV and PVI could be used to predict intraoperative fluid responsiveness during resection of PRPT in Hans Chinese.

Non-tuberculous mycobacterial infections of the skin: a retrospective study of 29 cases.

The incidence of infections caused by non-tuberculous mycobacteria has increased in recent years, due to a rise in dermatological procedures and a greater prevalence of immunosuppression in the general population. This study investigated the clinical and microbiological findings of non-tuberculous mycobacterial skin infections. The study population included 29 patients from whom non-tuberculous mycobacteria were cultured after isolation from skin biopsy materials, cutaneous abscesses or exudates. Clinical, microbiological and epidemiological data were collected from each patient. Eight patients were immunocompromised while 21 were not. Precipitating factors such as acupuncture, filler injection, surgical procedures and other traumatic events preceded infection in 13 (including 11 normal hosts and two immunocompromised hosts) of the 29 patients. Multiple skin lesions were present in eight patients (including three normal hosts and five immunocompromised hosts). In eight patients (including four immunocompromised hosts), symptoms were accompanied by tenosynovitis, osteomyelitis and myositis. Mycobacterium abscessus was isolated from nine patients, Mycobacterium fortuitum was isolated from nine patients, Mycobacterium chelonae was isolated from six patients, Mycobacterium marinum was isolated from two patients, a Mycobacterium avium complex member was isolated from two patients, and Mycobacterium haemophilum was isolated from one patient. Ten of the 24 cases caused by rapidly growing organisms (i.e. M. chelonae, M. abscessus and M. fortuitum groups) were precipitated by skin injuries such as acupuncture, filler infection and other medical procedures. Increases in skin medical procedures, including both acupuncture and esthetic interventions, explain the increasing incidence of these organisms. Immunocompromised patients tended to develop multiple skin lesions and deep tissue infections.