Background. Despite well‐established surgical approaches, the prognosis for patients with squamous cell carcinoma of the esophagus remains dismal. To assess the benefit of adjuvant chemotherapy and radiation therapy (CRT), a randomized trial with and without sequential preoperative CRT was undertaken; CRT combined 20 Gy and two courses of 5‐FU and cisplatin. Methods. Patients were included on the basis of the following criteria: squamous cell carcinoma of the esophagus, younger than 70 years of age, World Health Organization status below 2, estimated survival time greater than 3 months, and no previous treatment for the cancer. Patients were not included if they had experienced a loss in body weight greater than 15% or had tracheoesophageal fistula, metastases, or uncontrollable infection. Results. Eighty‐six patients thus fulfilled the criteria for inclusion (41 CRT, 45 non‐CRT). The groups were well‐matched for age, sex, tumor location, size, and grade. Operative mortality was 8.5% and 7%, respectively, for each group with a 27‐day hospital stay for both groups. Long‐term survival was not significantly different, with 47% of both groups alive at 1 year. Conclusions. The authors concluded that this neoadjuvant treatment did not change operative mortality or survival time for patients with squamous cell carcinoma of the esophagus.

A prospective randomized trial of 67 patients undergoing oesophagectomy by either a transhiatal approach or right-sided thoracotomy was conducted over a 40-month period. In 32 patients the approach was transhiatal and 35 had a thoracotomy; the groups were well matched before operation. There were two hospital deaths in patients having the transhiatal oesophagectomy and three in those undergoing thoracotomy. Blood transfusion, intensive care stay and overall time of hospitalization were not significantly different between the two groups. There was no difference in the postoperative morbidity rate and, in particular, the incidences of pulmonary complications were similar (19 per cent for transhiatal oesophagectomy, 20 per cent for thoracotomy) with anastomotic fistula in 6 and 9 per cent respectively. The median (range) operating time was significantly longer in patients having thoracotomy (6 (3.5-9.5) versus 4 (3-8) h). Long-term survival was unaffected by the type of operation performed or addition of preoperative chemotherapy or radiotherapy. Nodal status was a significant prognostic factor within but not between the two groups. It is concluded that oesophagectomy by a transhiatal route or right thoracotomy are equally effective surgical options for treatment of squamous cell oesophageal cancer.

In a randomized, double-blinded study, we evaluated the analgesic effect of ketamine in the management of pain in a surgical intensive care unit after major abdominal surgery. Patients received morphine patient-controlled analgesia with either placebo (Group M) or ketamine (Group K). Morphine was administered with initial loading doses of 2 mg until the visual analog scale (VAS) score was <30 and thereafter with bolus doses of 1 mg and a lockout time of 7 min. Ketamine was administered with an initial bolus of 0.5 mg/kg followed by a perfusion of 2 micro g x kg(-1) x min(-1) during the first 24 h and 1 micro g x kg(-1) x min(-1) during the following 24 h. The 4-h cumulative morphine doses were measured over 48 h. The VAS scores at rest and at mobilization were measured every 4 h during 48 h. A total of 101 patients were enrolled, and 93 were analyzed (41 in Group K and 52 in Group M). VAS scores at rest and at mobilization were similar. The cumulative consumption of morphine was significantly smaller in Group K (P < 0.05). We concluded that small doses of ketamine were a valuable adjunct to opioids in surgical intensive care unit patients after major abdominal surgery.

No abstract

Type XVIII collagen is a recently discovered nonfibrillar collagen associated with basement membranes in mice and expressed at high levels in human liver. We studied the origin, distribution, and RNA levels of type XVIII collagen in normal and fibrotic human livers by in situ hybridization, immunohistochemistry, and Northern and dot blots and compared procollagen ␣1(XVIII) RNA levels with those of procollagen ␣1(IV) and laminin ␥1, the two major components of liver basement membranes. In normal liver, type XVIII collagen was heavily deposited in perisinusoidal spaces and basement membrane zones. The major source of type XVIII collagen was hepatocytes and, to a lesser extent, endothelial, biliary epithelial, and vascular smooth muscle cells and peripheral nerves. In cirrhosis, type XVIII collagen formed a thick deposit along capillarized sinusoids. Grain counts after in situ hybridization showed myofibroblasts to increase their expression 13-fold in active and twofold in quiescent fibrosis, whereas hepatocytes increased their expression only twofold in both active and quiescent fibrosis. Activated stellate cells in vitro expressed type XVIII collagen at high levels. These data indicate that type XVIII collagen is a component of the perisinusoidal space and is associated with basement membrane remodeling. Hepatocytes and activated stellate cells are important sources of type XVIII collagen in normal and fibrotic liver respectively, which suggests tissue-specific regulation of its expression. (HEPATOLOGY 1998;28:98-107.)The collagen superfamily comprises at least 19 molecules that share repeating -Gly-X-Y-sequences and fold into triplehelical structures. 1,2 Specific collagen types arrange within extracellular matrices in precise aggregates, maintaining a delicate equilibrium in specialized tissues. 1,3,4 In the liver, collagen breakdown and deposition occur in fibrosis and cirrhosis as a result of the cooperation of injured or regenerating hepatocytes with stellate cells. Activated stellate cells are a major source of extracellular matrix proteins in fibrotic liver. 5-10 Indeed, upon activation during liver injury, stellate cells undergo phenotypic changes characteristic of myofibroblasts, express ␣-smooth muscle actin (␣-SMA), and produce extracellular matrix components at high levels. 11,12 The newly discovered type XVIII collagen [13][14][15] belongs to the nonfibrilar collagens, with frequent interruptions in the triple-helical structure, which possibly confer flexibility to the molecules. Type XVIII collagen is present in highly vascularized organs such as the liver, lung, kidney, and placenta. [16][17][18] Muragaki et al. 17 detected type XVIII collagen in vascular basement membrane zones in mice, and it has been hypothesized that this collagen type could be a new component of basement membranes, 19 the highly specialized extracellular matrices underlying epithelial or endothelial cells and surrounding muscle cells, fat, and peripheral nerve cells. Three variant N-terminal ends for mouse procollagen ␣1(XVIII...