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 investigate the effect of dexmedetomidine hydrochloride ( Dex ) preconditioning on renal function in rats after renal ischemia reperfusion injury under high glucose condition. Methods SD rats were randomly divided into 6 groups:NG-Sham operated group,NG-I/R group, NG-Dex group,HG-Sham operated group,HG-I/R group,HG-Dex group. Renal ischemia reperfusion model was established except Sham groups. Dex 50 μg·kg-1 was injected intraperitoneally 30 min before ischemia in the Dex preconditioning group,25% glucose 3 g·kg-1 was given intraperitoneally before the renal ischemia reperfusion model was established in high glucose groups. Blood glucose and renal function of each group were detected . Renal pathologic changes were observed with hematoxylin-eosin staining. Apoptosis of renal tissue was detected by TUNEL method. Results BUN,Cr and apoptosis rate in NG-I/R group were higher than those in NG-Sham operated group ( P<0.05);BUN,Cr and apoptosis rate in NG-Dex group were lower than those in NG-I/R group ( P<0.05);BUN,Cr and apoptosis rate in HG-I/R group and HG-Dex group were higher than those in NG-I/R group and NG-Dex group,respectively (P<0.05); However,there was no significant difference between HG-I/R group and HG-Dex group ( P>0.05) . Conclusion Dex has a protective effect on renal function after renal ischemia reperfusion, but this effect is inhibited in high glucose condition, which may relate to the increasing of kidney cells apoptosis.