Mucinous cystadenocarcinoma of the appendix. A rare tumour of the right iliac fossa

A case of mucinous cystadenocarcinoma of the appendix is presented. The clinical feature is a painful syndrome of the right iliac fossa. In our observation, the diagnosis was not allowed by preoperative imaging. Appendectomy was initially performed and completed by right hemicolectomy and lymphadenectomy after histological diagnosis of the appendicular malignant tumour was forwarded. The prognosis of this tumour is generally excellent providing early diagnosis and wide enough surgery.     

Application of the ion pair concept to the n-octanol-water partitioning of cefepime and cefpirome

The ion pair concept was applied for the assessment of lipophilicity of cefepime and cefpirome. Octanol-water distribution coefficients were determined in presence of different concentrations [X-] of sodium octanesulphonate. The log Dx values within the linear part of the log Dx/[X-] relationships were extrapolated to log Do values corresponding to the partitioning in absence of the counter ion. Measurements were feasible at pH values close to the isoelectric points of the acidic and basic functions. In that pH range the conduction of the experiments in presence of the hydrophobic counter anion facilitated the partitioning of the two cephalosporins to octanol, circumventing the problems arising from their high hydrophilicity. This procedure could not be applied at lower pH, possibly due to a further drastic decrease in the 'intrinsic' lipophilicity or to reduced ion pairing potential of octanesulphonate, and at higher pH due to the disruption of the zwitterionic structure. Extrapolated log Do values were compared to actual log D measurements performed for a reference quinolinium compound and for cefpirome. Extrapolated retention factors log kw close to the isoelectric point were also determined by reversed phase HPLC and compared to the log Do values.     

Differential regulation of VEGF, HIF1alpha and angiopoietin-1, -2 and -4 by hypoxia and ionizing radiation in human glioblastoma

We examined how ionizing radiation (IR) delivered under either severe hypoxia (< 0.1% O2) or normoxia affects the expression of hypoxia inducible factor 1alpha (HIF-1alpha) and the angiogenic factors vascular endothelial growth factor (VEGF) and angiopoietins 1, 2 and 4 in U87 human glioblastoma cells. IR was delivered as single doses of 0, 2, 5, 10 and 20 Gy after 6-hr hypoxic incubation and in normoxic controls. Irradiation at any dose did not affect the cellular protein levels of any of the angiopoietins, whereas hypoxia led to increasing levels of both angiopoietin-4 and angiopoietin-2. Levels of angiopoietin-1 protein were unaltered throughout the observation period. A dose-dependent increase in levels of secreted VEGF in the medium occurred after IR at doses from 5-20 Gy. In hypoxic cells, 20 Gy IR induced an additional significant increase in VEGF relative to nonirradiated hypoxic control cells with elevated baseline VEGF levels induced by hypoxia. HIF-1alpha and glucose transporter-1 (Glut-1) were not correspondingly upregulated by IR. Blocking HIF-1alpha by antisense treatment induced a reduced baseline VEGF at normoxia, while the relative upregulation of VEGF by IR was unaffected. These data provide evidence that VEGF is upregulated by IR by mechanisms independent of HIF-1 transactivation.     

Use of genetically engineered transgenic mice to investigate the role of galanin in the peripheral nervous system after injury

The neuropeptide galanin is present at high levels within the dorsal root ganglia (DRG) and spinal cord during development and after peripheral nerve damage in the adult. This pattern of expression suggests that it may play a role in the adaptive response of the peripheral nervous system (PNS) to injury. Several experimental paradigms have demonstrated that galanin modulates pain transmission, particularly after nerve injury. In our laboratory we have used a transgenic approach to further elucidate the functions of galanin within the somatosensory system. We have generated mice which over-express galanin (either inducibly after nerve injury, or constitutively), and knock-out (KO) mice, in which galanin is absent in all cells, throughout development and in the adult. Analysis of the nociceptive behaviour of the galanin over-expressing animals, before and after nerve injury, supports the view that galanin is an inhibitory neuromodulator of spinal cord transmission. In apparent contradiction to these findings, galanin KO animals fail to develop allodynia and hyperalgesia after nerve injury. However, further studies have shown that galanin is critical for the developmental survival of a subset of small diameter, unmyelinated sensory neurons that are likely to be nociceptors. This finding may well explain the lack of neuropathic pain-like behaviour after injury in the KO animals. Furthermore, the developmental survival role played by galanin is recapitulated in the adult where the peptide is required for optimal neuronal regeneration after injury, and in the hippocampus where it plays a neuroprotective role after excitotoxic injury.     

Plasma YKL-40, as a prognostic tumor marker in recurrent ovarian cancer

BACKGROUND: YKL-40, a member of family 18 glycosyl hydrolases, is secreted by cancer cells. The function of YKL-40 in cancer diseases is unknown, but it is a growth factor of connective tissue cells and probably has a role in inflammation and remodeling of the extracellular matrix, a process also involved in metastatic malignant diseases. High serum YKL-40 has been associated with poor prognosis for patients with colorectal and recurrent breast cancer. AIM OF THE STUDY: The purpose of the present study was to examine the prognostic value of plasma YKL-40 in patients presenting with recurring ovarian cancer. METHODS: YKL-40 was determined by ELISA in plasma samples from 73 patients with relapse of ovarian cancer shortly before start of second-line chemotherapy. The endpoint used was death because of ovarian cancer. RESULTS: Plasma YKL-40 was increased in ovarian cancer patients (median 94 micro g/L, range 20-1970 micro g/L) compared with age-matched controls (33 micro g/L, range 20-130 micro g/L) (p < 0.001). Fifty-five per cent of the patients had a plasma YKL-40 level above the upper normal 95th percentile of controls. Patients with high plasma YKL-40 (i.e. > 130 micro g/L or > 160 micro g/L) at the time of relapse had significantly shorter survival than patients with normal levels (respectively p = 0.007 and p = 0.004). Plasma YKL-40 proved to be an independent prognostic factor in a multivariate Cox analysis (YKL-40 > 160 micro g/L; HR = 2.27) (p = 0.006), including serum CA-125 and clinical/histological parameters. CONCLUSION: High plasma YKL-40 is related to short survival in patients with recurrent ovarian cancer.     

Novel HLA-A*31 allele, A*3111 identified by sequence-based typing

In this report, we describe the identification of an HLA-A*31 nucleotide sequence variant, a new HLA-A*3111, in three members of a Korean family by using sequence-based typing (SBT). The new allele was detected during routine HLA typing by high-resolution SBT. Allele A*3111 showed one nucleotide difference with A*310102 at codon 165 (GTG-->CTG) resulting in an amino acid change from valine to leucine (V165L). Serologic reactivity was shorter than normally expected.     

Unbalanced t(4;11)(q32;q23) in a 34-year-old man with manifestations of distal monosomy 11q and trisomy 4q syndromes

We present a 34-year-old man with an unbalanced translocation between the long arms of chromosome 4 and chromosome 11. He had manifestations of monosomy 11(q23)—minor facial anomalies, abnormal head shape, cryptorchidism; trisomy 4(q32)—hirsutism, renal disease; and manifestations attributable to both imbalances—heart disease, musculoskeletal anomalies, and mental retardation. FISH studies showed that the chromosome 11q23.3 translocation breakpoint was distal to the rare folate sensitive fragile site (FRA11B). The patient is the oldest reported with both imbalance of 4q+ and 11q-. Am. J. Med. Genet. 70:357–360, 1997. © 1997 Wiley-Liss, Inc.