Treatment of congenital cystic adenomatoid malformation-does resection in the early postnatal period increase surgical risk?

OBJECTIVE: The recent development of fetal ultrasonography has allowed for an increasing number of prenatal diagnoses for congenital cystic adenomatoid malformation (CCAM). However, the appropriate surgical timing of these patients has not been studied as of yet. The aim of this study is to suggest a safe strategy for the treatment of CCAM by identifying the relationship between the timing of surgery and postoperative outcome. METHODS: Between 1987 and 2003, 40 patients (28 males, 12 females) underwent surgical resection for CCAM. The mean age was 38.6+/-9.1 (2 days-13 years) months. CCAM was diagnosed by prenatal ultrasonography in eight patients. Early operations were performed in four out of the eight. Operation was deferred until 2-12 months of age for the remaining four patients. RESULTS: Type I CCAM was found in 20 patients, type II in 20 and no patient exhibited type III. Five patients had associated pectus excavatum anomaly. There were no cases of operative mortality. Seventeen minor postoperative complications developed in 16 patients (40.0%): prolonged chest tube drain in 10, wound infection in 4, and 1 case of pneumonia, empyema and pleural space, respectively. The average hospital stay was 11.8 (6-29) days. During the mean follow-up period of 67.5 months, one patient died of accidental aspiration 7 months after operation during the postoperative recovery course of Ravich operation for pectus excavatum. The remaining patients reported doing well with normal physical activity. All five patients who underwent surgery at the age of under 1 month did not exhibit increased postoperative morbidity. CONCLUSIONS: We concluded that surgery for CCAM could be safely performed in all age groups with satisfactory long-term outcomes. It is suggested that early elective surgical correction can be recommended for a patient whose diagnosis was made in utero.     

对耳轮过度前突畸形的整复

对耳轮过度前突为对耳轮的角度过锐，致使耳轮的位置相应后移，表现为与招风耳完全相反的畸形。畸形虽不十分明显，但影响美观。自１９９２年４月开始应用患侧耳廓软骨和耳后皮瓣对５例患者８只外耳进行治疗得到满意效果。认为文中所述方法是矫正对耳轮过度前突畸形的良好方法。     

Thymidine labeling index in breast tumors

The relationship between primary tumor proliferative activity and clinical and pathologic characteristics was analyzed in relation to menopausal status in 32 patients with malignant or benign breast disease. The thymidine labeling index (TLI) showed significantly higher median values in the cancer patients (3.48 per cent) than in the patients with benign diseases (1.02 per cent). TLI was not significantly affected by delayed incubation at room temperature for about 1 hour. In the breast cancer patients, TLI did not significantly correlate to tumor size, the presence of axillary lymph node metastasis or pathologic nuclear grading. The only significant difference was limited to the breast cancer patients without axillary lymph node metastasis in relation to menopausal status; the TLI in the premenopausal patients (5.10 per cent) was significantly higher (p<0.05) than that in the postmenopausal patients (2.28 per cent). These data thus suggest that among premenopausal patients without axillary lymph node metastasis, those with a high TLI could be potential candidates for adjuvant chemotherapy.     

High susceptibility of analbuminemic rats to neurogenic tumor induction by transplacental administration of N-ethyl-N-nitrosourea.

The susceptibilities of Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR) to N-ethyl-N-nitrosourea (ENU) were compared. In Experiment I, the rats were given daily subcutaneous injections of 10 mg/kg of ENU for a week from 4 weeks of age. In Experiment II, mother rats were given a single subcutaneous injection of 60 mg/kg of ENU on day 17 of pregnancy and tumor development in their offspring was examined. In Experiment I, the incidence of neurogenic tumors was slightly, but not significantly, higher in NAR than in control rats. In Experiment II, the incidence of total tumors including neurogenic tumors was significantly higher in NAR (40/43, 93.0%) than in SDR (13/61, 21.3%). NAR showed particularly high susceptibility to induction of neurogenic tumors (34/43, 79.1%) and renal tumors (15/43, 34.9%). In an attempt to elucidate the underlying mechanisms of the increased susceptibility of NAR to ENU, O6-ethylguanine, a major premutagenic ethylated DNA adduct, was quantitated in fetal brain DNA of NAR and SDR after a pulse exposure to 60 mg/kg ENU. No significant difference in the initial formation or subsequent repair of O6-ethylguanine was observed in the two strains, indicating that abnormality at some later stage(s) of chemical carcinogenesis may lead to the increased susceptibility of NAR to induction of neurogenic tumors.     

Toxicity associated with iron overload found in hemochromatosis: possible mechanism in a rat model.

Hemochromatosis is characterized by pathologic iron overload which often leads to various pathological conditions. The mechanism by which excess iron induces these conditions is not clearly understood. Using rats as the model, this investigation was conducted to explore the mechanism of toxicity associated with iron overload. Sprague-Dawley male rats were fed a 3% carbonyl iron-supplemented diet for eight weeks to achieve iron accumulation. Liver iron reached approximately 2 mg/g which is more than 16 times the control values (mean +/- SD, 0.12 +/- 0.02 mg/g, p < 0.001). Serum iron was consistently higher in the experimental rats (mg/L): 3.41 +/- 0.58 versus 1.89 +/- 0.18, p < 0.001. The high levels of iron accompanied enhanced oxidative damage in the hepatic nuclear DNA when 8-hydroxy-2'-deoxyguanosine (8-OHdG) was measured as a product of DNA oxidation. The levels of 8-OHdG in the experimental samples were significantly higher than the controls (8-OHdG X 10(-5)/dG): 4.22 +/- 1.82 versus 1.84 +/- 0.33, p < 0.05. The results of serum enzyme assays suggest that iron overload caused mild hepatocellular damage: alanine transaminase significantly increased; lactate dehydrogenase did not change; alkaline phosphatase decreased. Since the accumulation of 8-OHdG in the nuclear DNA is highly deleterious to cells, these data suggest oxidative damage in the nuclear DNA may be a critical factor in inducing diseases associated with iron overload.     

肠外营养对呼吸功能不全患者的影响

从加强医疗病房的重危患餐巾选取因呼吸衰竭而给予呼吸机支持的患者40例,随机分为A组20例进行肠外营养(parenteral nutrition,PN)治疗,B组20例未行PN治疗。对通气/换气功能各指标进行分析,结果两组患者的呼吸频率、pH、PaO_2、PaCO_2及HCO_3~-无明显差异;A组氧分压与吸入气氧浓度比值轻度降低,而肺泡-动脉氧压差及肺内分流明显升高。提示PN中的脂肪乳和高糖可能是导致呼吸功能改变的重要因素。     

Ⅰ期非小细胞肺癌淋巴结微转移规律的研究

目的探讨几个问题：（1）Ⅰ期非小细胞肺癌淋巴结微转移比率；（2）淋巴结微转移与肿瘤大小、病理类型、细胞分化程度、部位、分型、分期进行Logstic回归分析，确定影响微转移的主要因素；（3）探讨微转移的方式、顺序。方法对91例非小细胞肺癌清扫的肺门和隆突下淋巴结进行MCK（AEI／AE3）免疫组化标志检测微转移的存在。另外收集45例肺部良性病变手术时切除的肺门淋巴结45枚和Ⅱ期、Ⅲ期肺癌常规病理检查阳性的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化（SP法）标志，分别作为阴性和阳性对照。结果45例肺部良性病变手术时切除的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化标志均为阴性；Ⅱ期和Ⅲ期常规病理检查阳性的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化标志均为阳性。91例Ⅰ期非小细胞肺癌总的微转移率为49％（45／91）。结论Ⅰ期非小细胞肺癌淋巴结中存在微转移；Ⅰb期非小细胞肺癌微转移率明显高于Ⅰa期；有必要对Ⅰb期非小细胞肺癌进行术后化疗；肿瘤分期和分化程度是影响淋巴结微转移的主要因素；淋巴结微转移遵循肺门到纵隔的途径；腺癌存在跳跃式微转移。     

Poxvirus-based vaccine therapy for patients with advanced pancreatic cancer

Purpose  

An open-label Phase 1 study of recombinant prime-boost poxviruses targeting CEA and MUC-1 in patients with advanced pancreatic cancer was conducted to determine safety, tolerability and obtain preliminary data on immune response and survival.     

A phenytoin-sensitive cationic current participates in generating the afterdepolarization and burst afterdischarge in rat neocortical pyramidal cells

We report here on the ionic mechanisms underlying the depolarizing afterpotential (DAP) in neocortical pyramidal cells, with special interest in those underlying the burst afterdischarge. Injections of short depolarizing current pulses under whole-cell current clamp with a CsCl-based internal medium generated, in most pyramidal cells, a single action potential with a plateau phase (plateau-AP), followed by a slowly decaying DAP both in the absence and presence of TTX. Under voltage-clamp, the same cells displayed a slow tail current (tail-I) at the offset of depolarization. When intracellular free Ca²⁺ was chelated with 10 mm BAPTA or when extracellular Ca²⁺ was replaced with equimolar Ba²⁺, neither the slow DAP nor the slow tail-I was observed. Extracellular application of Co²⁺ or Cd²⁺ reduced Ca²⁺ currents and the slow tail-I. Cation substitution experiments revealed that the channel generating the slow tail-I was permeable to K⁺ and Cs⁺ more than to Na⁺ (P_K≈P_Cs > P_Na > P_NMDG≈P_TEA). The cationic slow tail-I was not reduced by applying antagonists of the metabotropic glutamate receptor (MCPG, 1 mm ) and the muscarinic receptor (atropine, 1–10 μm ). Thus, the slow DAP was produced by activation of the cationic channel whose gating is solely dependent on [Ca²⁺]_i. An increase in [K⁺]_o from 3 to 6 or 9 mm enhanced the slow DAP, and resulted in a generation of burst afterdischarges. An anticonvulsant, phenytoin (PT; 1–10 μm ) suppressed the slow DAP while enhancing the plateau-AP in the presence of TTX, most likely by blocking the cationic channel.