Objective To study the clinical value of PgCO_2 measurement on the patients in ICU.Methods PgCO_2 were continuous measured 24 hours by using air-automated tonometry for 50 cases admitted in ICU.The heart rate,blood pressure,MAP,CVP,SpO_2,artery blood gas were measured at the same time.According to acute physiologic and chronic health evaluation(APACH Ⅱ) and MODS mark,the patients were divided into 2 groups,high-risk group and light-risk group.20 cases suffered from malignant tumour without functional failure of the organs were looked on as compared group.The results of measurement of every group were compared.Results Comparing with the three groups,the results of PgCO_2,Pg-aCO_2,Pg-etCO_2 were significantly different,but the Pg-aCO_2 and Pg-etCO_2 were the same.Conclusion PgCO_2 is an effective index for observing the conditional change of the high-risk cases.PgCO_2≥45mmHg,Pg-aCO_2≥15mmHg may be considered as a predictive signal that the patient well appears functional failure or death.Pg-etCO_2 may substitute Pg-aCO_2 as a continuous measurement index.

Objective:To investigate the effect of different ventilation time in the prone position on patients with endogenous/exogenous ARDS.Methods:30 endogenous/30 exogenous ARDS patients were randomly devided into 4 groups,ventilation in the prone position for 2 h and 4 h.Recording the score of APCHEII,oxygenation index,the absorption situation in X-ray,HR,MAP,extubation time,the time out of ICU.Results:The APCHEII scores HR and MAP in four groups have no significant statistics (P＞0.05);4h ventilation for endogenous ARDS patients has a better indicators than 2 h in oxygenation index,the absorption situation in X-ray,extubation time and the time out of ICU (P＜0.05);2 h and 4 h ventilation for exogenous ARDS patients can improve indicators above,two groups have no significant statistics (P＞0.05),the results of exogenous groups are precede than endogenous group (P＜0.05).Conclusion:Ventilation in the prone position can improve the situation of ARDS patients,both endogenous patients and exogenous patients.Exogenous ARDS patients have a better treatment effect after the ventilation of 2h,however,endogenous patients need longer time and have a non-ideal prognosis.

Background and purpose:Cancer-related pain is one of the most important symptoms of patients with advanced cancer. Chemotherapy sometimes induces peripheral neuropathy and pain. These symptoms seriously affect patients’ quality of life. Cancer pain assessment is now achieved by the subjective scales of patients, but lacking objective measurement. In this study, we used the neurotic electrophysiological method by way of PainVision system (PV system) to evaluate cancer pain quantitatively to detect and analyze degree of chemotherapy-induced neuropathy. Methods:We obtained numerical rating scale (NRS) scores from patients receiving analgesics and calculated the PainRatio from PV system at the same time. Then we analyzed the relationship between NRS and PainRatio scores. We detected current perception threshold (CPT) levels of patients receiving chemotherapy to ifnd the correlation between chemotherapy and CPT level, and attempt to evaluate chemotherapy-induced neuropathy.Results:PainRatio scores were linearly associated with NRS scores (Pearson correlation coeffcient=0.849,P<0.001). Patients with neuropathy symptoms got higher CPTs. However, no statistically signiifcant difference was observed between patients treated with oxaliplatin, paclitaxel and other agents.Conclusion:PainVision system can be used in cancer pain assessment quan-titatively, and be helpful in cancer pain assessment objectively. Patients with deifned neuropathy showed higher CPTs, indicating the potential clinical value of PV system in detecting and evaluating chemotherapy-induced neuropathy.

Objective To investigate the value of remnant stomach-jejunal dual pathways reconstruction after laparoscope-assisted radical proximal gastrectomy in the treatment of upper gastric cancer. Methods Twenty-five patients with upper gastric cancer underwent laparoscope-assisted radical proximal gastrectomy and the remnant distal stomach was preserved for side-to-side remnant stomach-jejunal anastomosis and end-to-side jejuno-jejunal anastomosis to reconstruct dual pathways. Results The mean operation time was (240±35) minutes, the mean number of lymph nodes dissected were 22±5, and all the incised margins were negative. No anastomotic leakage, obstruction or stenosis occurred. All patients received postoperative barium meal examination. A large amount of barium directly entered the jejunum, leaving a small amount of barium entered the jejunnum via the route of remnant stomach-duodenum, and was detained in the remnant stomach for 30-60 minutes. No esophageal reflux of barium was observed. All the patients were followed up for 4-18 months, no reflux esophagitis was detected and the short-term life quality was satisfactory. Conclusions Remnant stomach-jejunal dual pathways reconstruction prevents the reflux esophagitis and dumping syndrome, preserves the pathway of duodenum and promotes the life quality of patients.

Colorectal cancer ranks third in global incidence and is the second leading cause of cancer-related mortality. Doxorubicin, an anthracycline chemotherapeutic drug, is integral to current cancer treatment protocols. However, toxicity and resistance to doxorubicin poses a significant challenge to effective therapy. Panobinostat has emerged as a critical agent in colorectal cancer treatment due to its potential to overcome doxorubicin resistance and enhance the efficacy of existing therapeutic protocols. This study aimed to evaluate the capability of panobinostat to surmount doxorubicin toxicity and resistance in colorectal cancer. Specifically, we assessed the efficacy of panobinostat in enhancing the therapeutic response to doxorubicin in colorectal cancer cells and explored the potential synergistic effects of their combined treatment. Our results demonstrate that the combination treatment significantly reduces cell viability and colony-forming ability in colorectal cancer cells compared to individual treatments. The combination induces significant apoptosis, as evidenced by increased levels of cleaved PARP and cleaved caspase-9, while also resulting in a greater reduction in p-Akt/p-GSK-3β/mTOR expression, along with substantial decreases in c-Myc and SREBP-1 levels, compared to monotherapies. Consistent with the in vitro experimental results, the combination treatment significantly inhibited tumor formation in colorectal cancer xenograft nude mice compared to the groups treated with either agent alone. In conclusion, our research suggests that the panobinostat effectively enhances the effect of doxorubicin and combination of two drugs significantly reduced colorectal cancer tumor growth by targeting the Akt/ GSK-3β/mTOR signaling pathway, indicating a synergistic therapeutic potential of these two drugs in colorectal cancer treatment.

Colorectal cancer ranks third in global incidence and is the second leading cause of cancer-related mortality. Doxorubicin, an anthracycline chemotherapeutic drug, is integral to current cancer treatment protocols. However, toxicity and resistance to doxorubicin poses a significant challenge to effective therapy. Panobinostat has emerged as a critical agent in colorectal cancer treatment due to its potential to overcome doxorubicin resistance and enhance the efficacy of existing therapeutic protocols. This study aimed to evaluate the capability of panobinostat to surmount doxorubicin toxicity and resistance in colorectal cancer. Specifically, we assessed the efficacy of panobinostat in enhancing the therapeutic response to doxorubicin in colorectal cancer cells and explored the potential synergistic effects of their combined treatment. Our results demonstrate that the combination treatment significantly reduces cell viability and colony-forming ability in colorectal cancer cells compared to individual treatments. The combination induces significant apoptosis, as evidenced by increased levels of cleaved PARP and cleaved caspase-9, while also resulting in a greater reduction in p-Akt/p-GSK-3β/mTOR expression, along with substantial decreases in c-Myc and SREBP-1 levels, compared to monotherapies. Consistent with the in vitro experimental results, the combination treatment significantly inhibited tumor formation in colorectal cancer xenograft nude mice compared to the groups treated with either agent alone. In conclusion, our research suggests that the panobinostat effectively enhances the effect of doxorubicin and combination of two drugs significantly reduced colorectal cancer tumor growth by targeting the Akt/ GSK-3β/mTOR signaling pathway, indicating a synergistic therapeutic potential of these two drugs in colorectal cancer treatment.

Colorectal cancer ranks third in global incidence and is the second leading cause of cancer-related mortality. Doxorubicin, an anthracycline chemotherapeutic drug, is integral to current cancer treatment protocols. However, toxicity and resistance to doxorubicin poses a significant challenge to effective therapy. Panobinostat has emerged as a critical agent in colorectal cancer treatment due to its potential to overcome doxorubicin resistance and enhance the efficacy of existing therapeutic protocols. This study aimed to evaluate the capability of panobinostat to surmount doxorubicin toxicity and resistance in colorectal cancer. Specifically, we assessed the efficacy of panobinostat in enhancing the therapeutic response to doxorubicin in colorectal cancer cells and explored the potential synergistic effects of their combined treatment. Our results demonstrate that the combination treatment significantly reduces cell viability and colony-forming ability in colorectal cancer cells compared to individual treatments. The combination induces significant apoptosis, as evidenced by increased levels of cleaved PARP and cleaved caspase-9, while also resulting in a greater reduction in p-Akt/p-GSK-3β/mTOR expression, along with substantial decreases in c-Myc and SREBP-1 levels, compared to monotherapies. Consistent with the in vitro experimental results, the combination treatment significantly inhibited tumor formation in colorectal cancer xenograft nude mice compared to the groups treated with either agent alone. In conclusion, our research suggests that the panobinostat effectively enhances the effect of doxorubicin and combination of two drugs significantly reduced colorectal cancer tumor growth by targeting the Akt/ GSK-3β/mTOR signaling pathway, indicating a synergistic therapeutic potential of these two drugs in colorectal cancer treatment.

Colorectal cancer ranks third in global incidence and is the second leading cause of cancer-related mortality. Doxorubicin, an anthracycline chemotherapeutic drug, is integral to current cancer treatment protocols. However, toxicity and resistance to doxorubicin poses a significant challenge to effective therapy. Panobinostat has emerged as a critical agent in colorectal cancer treatment due to its potential to overcome doxorubicin resistance and enhance the efficacy of existing therapeutic protocols. This study aimed to evaluate the capability of panobinostat to surmount doxorubicin toxicity and resistance in colorectal cancer. Specifically, we assessed the efficacy of panobinostat in enhancing the therapeutic response to doxorubicin in colorectal cancer cells and explored the potential synergistic effects of their combined treatment. Our results demonstrate that the combination treatment significantly reduces cell viability and colony-forming ability in colorectal cancer cells compared to individual treatments. The combination induces significant apoptosis, as evidenced by increased levels of cleaved PARP and cleaved caspase-9, while also resulting in a greater reduction in p-Akt/p-GSK-3β/mTOR expression, along with substantial decreases in c-Myc and SREBP-1 levels, compared to monotherapies. Consistent with the in vitro experimental results, the combination treatment significantly inhibited tumor formation in colorectal cancer xenograft nude mice compared to the groups treated with either agent alone. In conclusion, our research suggests that the panobinostat effectively enhances the effect of doxorubicin and combination of two drugs significantly reduced colorectal cancer tumor growth by targeting the Akt/ GSK-3β/mTOR signaling pathway, indicating a synergistic therapeutic potential of these two drugs in colorectal cancer treatment.

Colorectal cancer ranks third in global incidence and is the second leading cause of cancer-related mortality. Doxorubicin, an anthracycline chemotherapeutic drug, is integral to current cancer treatment protocols. However, toxicity and resistance to doxorubicin poses a significant challenge to effective therapy. Panobinostat has emerged as a critical agent in colorectal cancer treatment due to its potential to overcome doxorubicin resistance and enhance the efficacy of existing therapeutic protocols. This study aimed to evaluate the capability of panobinostat to surmount doxorubicin toxicity and resistance in colorectal cancer. Specifically, we assessed the efficacy of panobinostat in enhancing the therapeutic response to doxorubicin in colorectal cancer cells and explored the potential synergistic effects of their combined treatment. Our results demonstrate that the combination treatment significantly reduces cell viability and colony-forming ability in colorectal cancer cells compared to individual treatments. The combination induces significant apoptosis, as evidenced by increased levels of cleaved PARP and cleaved caspase-9, while also resulting in a greater reduction in p-Akt/p-GSK-3β/mTOR expression, along with substantial decreases in c-Myc and SREBP-1 levels, compared to monotherapies. Consistent with the in vitro experimental results, the combination treatment significantly inhibited tumor formation in colorectal cancer xenograft nude mice compared to the groups treated with either agent alone. In conclusion, our research suggests that the panobinostat effectively enhances the effect of doxorubicin and combination of two drugs significantly reduced colorectal cancer tumor growth by targeting the Akt/ GSK-3β/mTOR signaling pathway, indicating a synergistic therapeutic potential of these two drugs in colorectal cancer treatment.

Objective To evaluate the role of thioredoxin?interacting protein(TXNIP)∕oligomer?ization domain?like receptor family pyrin domain?containing 3(NLRP3)signaling pathway in renal ische?mia?reperfusion(I∕R)injury in diabetic rats. Methods Pathogen?free healthy male Sprague?Dawley rats, aged 8-12 weeks, weighing 200-220 g, were used in the study. Diabetes mellitus was induced by intrap?eritoneal injection of 1% streptozotocin 65 mg∕kg and confirmed by blood glucose≥16.7 mmol∕L 3 days lat?er. Twenty?four diabetic rats were divided into 3 groups(n=8 each)using a random number table: sham operation group(group S), renal I∕R group(group I∕R)and resveratrol(TXNIP inhibitor)group (group R). Resveratrol 10 mg∕kg was intraperitoneally injected every day for 7 consecutive days starting from 3rd week after successful establishment of the model in group R. At 4th week after successful establish?ment of the model, renal I∕R was produced by occlusion of bilateral renal pedicles for 25 min followed by reperfusion in anesthetized rats in group R. The animals were sacrificed at 48 h of reperfusion, and renal specimens were obtained for microscopic examination of pathologic changes and for measurement of malondi?aldehyde(MDA)content, superoxide dismutase(SOD)activity and superoxide anion scavenging capa?bility(using colorimetric method), interleukin?1beta(IL?1β)and IL?18 contents(by enzyme?linked immunosorbent assay), cell apoptosis(using TUNEL)and expression of TXNIP, NLRP3 and caspase?1 in renal tissues(using Western blot). Blood samples were obtained from the left ventricle for determination of serum urea nitrogen(BUN)and creatinine(Cr)concentrations. Results Compared with group S, the serum Cr concentration and apoptosis index were significantly increased, superoxide anion scavenging capability in renal tissues was decreased, and the expression of TXNIP, NLRP3 and caspase?1 was up?reg?ulated in I∕R and R groups, and the serum BUN concentration and contents of MDA, IL?1β and IL?18 in renal tissues were increased, the SOD activity was decreased(P<0.05), and the pathological changes of renal tissues were aggravated in group I∕R. Compared with group I∕R, the serum BUN and Cr concentra?tions were significantly decreased, the contents of MDA, IL?1β and IL?18 and apoptosis index were de?creased, the SOD activity and superoxide anion scavenging capability were increased, the expression of TXNIP, NLRP3 and caspase?1 was down?regulated(P<0.05), and the pathological changes of renal tis?sues were significantly attenuated in group R. Conclusion The pathophysiological mechanism of renal I∕R injury is associated with the activation of TXNIP∕NLRP3 signaling pathway in diabetic rats.