Low-grade dietary-related inflammation and survival after colorectal cancer surgery

Purpose

Prolong inflammation is a central process observed in several chronic conditions and may be responsible for survival. There is an increasing evidence showing the role of diet in inflammation and habitual diet may be responsible for low-grade inflammation. The purpose of our study was to assess the effect of inflammatory properties of habitual diet measured by the Dietary Inflammatory Index (DII) on survival among surgical patients treated for colorectal cancer (CRC).

Methods

A follow-up study among 689 CRC patients (mean age 58 years, ±8.9; 56.7 % males) treated surgically was performed in Krakow, Poland. Habitual diet was assessed by a standardized semiquantitative food frequency questionnaire. Next, 23 dietary items were used to calculate DIIs. Vital records were verified to determine status of the participants.

Results

Study has shown linear association between DII and survival time among CRC patients with totally removed cancer treated by chemotherapy (b = ?0.13, p = 0.024). After adjustment for several important covariates, DII was associated with survival during up to 3 years after surgery, but only in patients without distant metastases (3-year HR_DII>?2.27 = 0.61, 95 % CI 0.38–0.99).

Conclusions

The results of the investigation have shown the usefulness of the DII as a potential predictor of survival among patients without distant metastases treated surgically for CRC.     

Structure and expression of genes of GM-CSF and G-CSF in blast cells from patients with acute myeloblastic leukemia

The hematopoietic growth factors granulocyte/macrophage colony- stimulating factor (GM-CSF) and G-CSF, available as recombinant products, stimulate the growth in culture of blasts from patients with acute myeloblastic leukemia (AML). We used cDNA probes for each gene to study the genomic organization in blast cells of 22 patients and expression in the blast cells of 18 patients. Alteration in the structure of G-CSF (two instances) and GM-CSF (two instances) was found. In two patients in whom it was possible to study DNA from bone marrow obtained at remission, the new bands detected in the leukemic cells were not found. Fifteen of 18 patients showed no RNA expression of either growth factor. Both patients with GM-CSF abnormalities as seen by Southern analysis expressed an abnormally large GM-CSF message but no G-CSF messages. One patient with an abnormal Southern pattern with G-CSF expressed normal-sized G-CSF and GM-CSF messages. The biologic significance of these findings remains to be determined. Nonetheless, the abnormal Southern patterns may prove to be useful clonal markers in the study of AML.     

A study to evaluate the first dose of gentamicin needed to achieve a peak plasma concentration of 30 mg/l in patients hospitalized for severe sepsis

Previous studies have shown that the high dose of gentamicin (8 mg/kg) rarely achieves the desired peak plasma concentration (Cmax) of ≥30 mg/l in patients with severe sepsis or septic shock. The aim of this study was to determine the first dose of gentamicin needed to achieve a Cmax ≥ 30 mg/l. We conducted a prospective observational cohort study in one intensive care unit. All consecutive patients hospitalized for severe sepsis or septic shock and treated with a first dose of gentamicin >6 mg/kg were evaluated. During the study period, 15 of the 57 patients (26.3 %) treated with gentamicin had a Cmax ≥ 30 mg/l. The median dose of gentamicin administered was 8.9 [7.8–9.9] mg/kg. Independent factors in the multivariate analysis associated with a Cmax ≥ 30 mg/l were higher body mass index (per kg/m² increment) (OR: 1.173, 95%CI: 1.015–1.356, P = 0.03) and higher first dose of gentamicin (per mg/kg increment) (OR: 2.343, 95%CI: 1.346–4.08, P = 0.003). The optimal first dose to achieve a Cmax ≥ 30 mg/l was 11 mg/kg, with a specificity and a sensitivity of 100 % and 53.3 % respectively. These results suggest that a first dose of gentamicin >11 mg/kg is needed to achieve a Cmax ≥ 30 mg/l in most patients.     

环丙沙星在预防酒精对肝细胞再生抑制中的作用

急性或慢性酒精中毒可不同程度抑制肝细胞ＤＮＡ合成和肝细胞再生。多数学者认为酒精抑制肝细胞再生与酒精抑制聚胺 (Ｐｏｌｙａｍｉｎｅ ,包括四甲烯二胺、精脒和精胍 )合成有关[1,2 ] 。实验证明 ,γ 氨基丁酸 (γ ａｍｉｎｏｂｕｔｙｒｉｃａｃｉｄ ,ＧＡＢＡ)是聚胺代谢的衍生物 ,是神经传递介质之一 ,是细胞增生调节中的抑制剂。Ｍｉｎｕｋ等[3 ] 指出 ,酒精中毒的实验动物血液中ＧＡＢＡ浓度升高 ,ＧＡＢＡ可能激活了肝脏ＧＡＢＡ受体 ,改变了细胞内环境。因此 ,酒精抑制肝脏合成聚胺可能是由于ＧＡＢＡ介导的结果。Ｄｉｅｈｌ[2 ] 认…     

The Role of Galanin in Cerebellar Granule Cell Migration in the Early Postnatal Mouse during Normal Development and after Injury

Galanin, one of the most inducible neuropeptides, is widely present in developing brains, and its expression is altered by pathologic events (e.g., epilepsy, ischemia, and axotomy). The roles of galanin in brain development under both normal and pathologic conditions have been hypothesized, but the question of how galanin is involved in fetal and early postnatal brain development remains largely unanswered. In this study, using granule cell migration in the cerebellum of early postnatal mice (both sexes) as a model system, we examined the role of galanin in neuronal cell migration during normal development and after brain injury. Here we show that, during normal development, endogenous galanin participates in accelerating granule cell migration via altering the Ca²⁺ and cAMP signaling pathways. Upon brain injury induced by the application of cold insults, galanin levels decrease at the lesion sites, but increase in the surroundings of lesion sites. Granule cells exhibit the following corresponding changes in migration: (1) slowing down migration at the lesion sites; and (2) accelerating migration in the surroundings of lesion sites. Experimental manipulations of galanin signaling reduce the lesion site-specific changes in granule cell migration, indicating that galanin plays a role in such deficits in neuronal cell migration. The present study suggests that manipulating galanin signaling may be a potential therapeutic target for acutely injured brains during development.SIGNIFICANCE STATEMENT Deficits in neuronal cell migration caused by brain injury result in abnormal development of cortical layers, but the underlying mechanisms remain to be determined. Here, we report that on brain injury, endogenous levels of galanin, a neuropeptide, are altered in a lesion site-specific manner, decreasing at the lesion sites but increasing in the surroundings of lesion sites. The changes in galanin levels positively correlate with the migration rate of immature neurons. Manipulations of galanin signaling ameliorate the effects of injury on neuronal migration and cortical layer development. These results shed a light on galanin as a potential therapeutic target for acutely injured brains during development.     

取代苄基/萘甲基异喹啉类及有关季铵衍生物的合成与生物活性

以具心血管活性的异喹啉类生物碱为先导物,结合某些钾通道阻滞剂的结构特征,设计合成了28个3,4-二氢(I_1～4)和1,2,3,4-四氢苄基/萘甲基异喹啉化合物(II_1～18)及有关季铵衍生物(I_5,6和II_19～22)。药理试验表明:除化合物I₄有一定升压作用外,大多化合物有不同程度的降压和减慢心率活性,其中化合物II1的降压活性最强。分析定量构效关系发现:化合物母核氮原子电荷愈大(即其绝对值愈小),降压作用愈强;反之,减慢心率作用愈强。异喹啉母核氮原子电荷可能为影响作用于血管或心脏组织的重要因素之一。     

Dural sinus thrombosis: study using intermediate field strength MR imaging

The magnetic resonance (MR) images of six patients with thrombosis of a dural sinus were reviewed. The diagnosis had been verified by computed tomographic scans in three patients and arteriograms in two; in the sixth patient, only MR imaging was used to confirm the clinical syndrome. In all patients, high-intensity signal was seen from the thrombus within the affected dural sinus on all echoes. This persistent signal intensity allowed intravascular clot to be distinguished from normal causes of increased signal such as flow-related enhancement (entry phenomenon) and even-echo rephasing. MR imaging demonstrated the cause of the thrombosis in three patients: two were secondary to adjacent tumors, and one was secondary to unsuspected mastoiditis. Complications such as infarction were also demonstrated. Using MR imaging, one can easily and safely diagnose thrombosis of a dural sinus. MR should be the imaging method of choice in patients suspected of having thrombosis of a dural sinus.     

Lactate and base deficit are predictors of mortality in critically ill patients with cancer

OBJECTIVE:

Cancer patients frequently require admission to intensive care unit. However, there are a few data regarding predictive factors for mortality in this group of patients. The aim of this study was to evaluate whether arterial lactate or standard base deficit on admission and after 24 hours can predict mortality for patients with cancer.

METHODS:

We evaluated 1,129 patients with severe sepsis, septic shock, or postoperative after high-risk surgery. Lactate and standard base deficit collected at admission and after 24 hours were compared between survivors and non-survivors. We evaluated whether these perfusion markers are independent predictors of mortality.

RESULTS:

There were 854 hospital survivors (76.5%). 24 h lactate >1.9 mmol/L and standard base deficit < -2.3 were independent predictors of intensive care unit mortality. 24 h lactate >1.9 mmol/L and 24 h standard base deficit < -2.3 mmol/Lwere independent predictors of hospital death.

CONCLUSION:

Our findings suggest that lactate and standard base deficit measurement should be included in the routine assessment of patients with cancer admitted to the intensive care unit with sepsis, septic shock or after high-risk surgery. These markers may be useful in the adequate allocation of resources in this population.