Lateral face reconstruction with the medial-based cervicopectoral flap

The problem of reconstructing large defects involving the lateral facial skin following extirpative surgery for cancer was ideally addressed by the use of the cervicopectoral flap. It has proved reliable, easy to fashion, and cosmetically acceptable; yet it does not interfere with sound oncologic principles for carcinoma resection in the head and neck. It has received little exposure in the literature and we feel it is an underutilized flap. No major complications are reported with this flap in our series of six patients.     

The response of immunologically reconstituted mice to allogeneic skin or tumour grafts

A study has been made of cytological and histological changes in lymph nodes draining grafts of allogeneic skin or tumour. The two types of graft provoked mitosis of both thymus- and bone-marrow-derived lymphocytes; this activity was associated with reactive changes initially in the paracortex and then in germinal centrts and medullary cords. Grafts of allogeneic skin evoked two peaks of mitosis which declined rapidly as the graft was rejected. Transient mitotic activity also occurred in response to (control) syngeneic skin, coinciding with increased lymph-node weight and some paracortical hyperplasia but (cf. changes found after allografting), other parts of the node did not respond. Allogeneic EL4 lymphoma cells gave rise to a greater and more rapid immunological response than did skin grafting. The mitotic response to the injected tumour cells failed, at least in the draining lymph nodes, long before death of the host due to progressive tumour growth. It is suggested that both the greater mitotic response, and its later failure, are related to the progressive growth of the tumour and to the everincreasing antigenic burden which such a tumour represents.     

Hyperpolarization of rabbit superior cervical ganglion cells due to activity of an electrogenic sodium pump

1 The mechanisms underlying the hyperpolarization which follows depolarization of rabbit superior cervical ganglion cells by acetylcholine, have been investigated and compared with the mechanisms responsible for the hyperpolarizations induced by orthodromic stimulation of the ganglion.2 The amplitude of the drug-induced hyperpolarization (after-hyperpolarization) was diminished when [Na(+)](0) and the duration of the preceding depolarization were reduced.3 In K(+)-free solutions, the amplitude of the after-hyperpolarization was often diminished and its rate of development was reduced. In 12.5 mM K(+)-Krebs solutions, the amplitude and rate of development of the after-hyperpolarization were increased; the potential was still present when the resting potential was at or close to E(K).4 Ouabain (10 muM) prevented or greatly diminished the after-hyperpolarization. The rates of onset and decay of the after-hyperpolarization were reduced in glucose-free solutions.5 It is, therefore, concluded that the after-hypolarization is due to the activity of an electrogenic sodium pump.6 The positive after-potential associated with the ganglionic action potential was increased in K(+)-free solutions and diminished when the resting potential approached E(K), indicating that it is due to a period of increased K(+) conductance. In the presence of high concentrations of hexamethonium (276 muM), the P wave was not selectively depressed by ouabain and has been shown by other workers to be due to a mechanism not involving an increased potassium conductance. It is concluded, therefore, that the positive after-potential, the P wave and the after-hyperpolarization are due to different mechanisms.     

A patient with sclerosing autoimmune pancreaticocholangitis as the cause of recurrent cholangitis following a pylorus-sparing pancreaticoduodenectomy

A pylorus-sparing pancreaticoduodenectomy was performed in a 67-year-old man because of indications for a carcinoma of the distal common bile duct. Histology of the postoperative specimen, however, revealed a sclerosing inflammation of the distal common bile duct and the surrounding pancreatic parenchyma. Initial postoperative recovery was followed by recurrent cholangitis. Stenosis of the choledocho-jejunostomy could not be demonstrated. Instead, repeated endoscopic retrograde cholangiopancreaticography revealed extensive sclerosis of the intrahepatic bile ducts, which suggested a sclerosing cholangitis associated with an autoimmune pancreatitis: sclerosing autoimmune pancreaticocholangitis. This disorder was recently described; it is characterised by a disorder in the pancreas that is indistinguishable from malignancy by imaging techniques and that is followed by a sclerosing inflammation of the bile ducts. The disease responds well to steroids. The patient described demonstrated a complete clinical and biochemical recovery after initiation ofprednisone therapy.     

Hypoglycemia masquerading as cerebrovascular disease (hypoglycemic hemiplegia)

Hypoglycemia produced hemiplegia with right-sided predilection in 16 patients initially suspected of having suffered a stroke. Fifteen patients had no demonstrable brain disease, and the hemiplegia cleared rapidly once the hypoglycemia was corrected. Invasive investigations such as carotid arteriography are not required in most patients. The features of hypoglycemia hemiplegia suggest that a selective neuronal vulnerability and not underlying focal brain disease is responsible in most cases.     

LH3, a "homologue" of the mastadenoviral E1B 55-kDa protein is a structural protein of atadenoviruses

Ovine adenovirus serotype 7 (OAdV), the prototype atadenovirus, has gene homologues for most mastadenovirus structural proteins but lacks proteins V and IX. Instead, OAdV has structural proteins of 32 and 42 kDa although the gene encoding the latter had not previously been identified. The presently reported studies of OAdV virions have now identified a minor structural polypeptide of approximately 40 kDa as the product of the L1 52/55-kDa gene and, more surprisingly, shown that the 42-kDa protein is encoded by LH3. This gene product was previously thought to be a homologue of mastadenovirus E1B 55 kDa, which is a multi-functional, non-structural protein that cooperates with E1A in cell transformation. The lack of transforming activity previously demonstrated for OAdV combined with a structural role for the LH3 product indicates that the protein has a different function in atadenoviruses. We discuss the abundance and likely core location of LH3 in the virion and the possible derivation of the E1B 55-kDa gene from the LH3 gene.