The use of water-jet dissection in open and laparoscopic liver resection

Background. We intend to give an overview of our experiences with the implementation of a new dissection technique in open and laparoscopic surgery. Methods. Our database comprises a total of 950 patients who underwent liver resection. Three hundred and fifty of them were performed exceptionally with the water-jet dissector. Forty-one laparoscopic partial liver resections were accomplished. Results. Using the water-jet dissection technique it was possible to reduce the blood loss, the Pringle- and resection time in comparison to CUSA® and blunt dissection. In the last five years we could reduce the Pringle-rate from 48 to 6% and the last 110 liver resections were performed without any Pringle''s manoeuvre. At the same time, the transfusion-rate decreased from 1.86 to 0.46 EC/patient. In oncological resections, the used dissection technique had no influence on long-time survival. Conclusions. The water-jet dissection technique is fast, feasible, oncologically safe and can be used in open and in laparoscopic liver surgery.     

Diagnosis of megacystis-microcolon intestinal hypoperistalsis syndrome with aplastic desmosis in adulthood: a case report

Megacystis-microcolon intestinal hypoperistalsis syndrome (MMHIS or Berdon syndrome) is an autosomal-recessive disorder characterized by chronic intestinal obstruction. Although the disease is often diagnosed in female infants we describe a man with late diagnosis in adulthood. Our patient presented soon after birth with intestinal obstruction and developed short bowel syndrome after multiple intestinal resections. Of note, the connective tissue net within the muscle layers of the intestinal wall was absent ('aplastic desmosis'). This case illustrates the variable clinical features of MMHIS and aplastic desmosis, which might delay the correct diagnosis of a severe disorder.     

Endobronchial metastasis from renal cell carcinoma: a case report

A 46-year-old man had primary pulmonary symptoms of intermittent fever, cough and dyspnoea. Radiological investigations revealed a mass at right hilum with right upper lobe collapse. Bronchoscopy showed a luminal mass of which the biopsy showed a tumour with predominantly clear cell change. Subsequent investigations revealed primary renal adenocarcinoma. The differential diagnosis of clear cell lung tumour is discussed. This case of endobronchial metastasis from renal cell carcinoma is being presented because of its rarity.     

Heat sensitization in skin and muscle nociceptors expressing distinct combinations of TRPV1 and TRPV2 protein

Recordings were made from small and medium diameter dorsal root ganglia (DRG) neurons that expressed transient receptor potential (TRP) proteins. Physiologically characterized skin nociceptors expressed either TRPV1 (type 2) or TRPV2 (type 4) in isolation. Other nociceptors co-expressed both TRP proteins and innervated deep tissue sites (gastrocnemius muscle, distal colon; type 5, type 8) and skin (type 8). Subpopulations of myelinated (type 8) and unmyelinated (type 5) nociceptors co-expressed both TRPs. Cells that expressed TRPV1 were excellent transducers of intense heat. Proportional inward currents were obtained from a threshold of approximately 46.5 to approximately 56 degrees C. In contrast, cells expressing TRPV2 alone (52 degrees C threshold) did not reliably transduce the intensity of thermal events. Studies were undertaken to assess the capacity of skin and deep nociceptors to exhibit sensitization to repeated intense thermal stimuli [heat-heat sensitization (HHS)]. Only nociceptors that expressed TRPV2, alone or in combination with TRPV1, exhibited HHS. HHS was shown to be Ca(2+) dependent in either case. Intracellular Ca(2+) dependent pathways to HHS varied with the pattern of TRP protein expression. Cells co-expressing both TRPs modulated heat reactivity through serine/threonine phosphorylation or PLA(2)-dependent pathways. Cells expressing only TRPV2 may have relied on tyrosine kinases for HHS. We conclude that heat sensitization in deep and superficial capsaicin and capsaicin-insensitive C and Adelta nociceptors varies with the distribution of TRPV1 and TRPV2 proteins. The expression pattern of these proteins are specific to subclasses of physiologically identified C and A fiber nociceptors with highly restricted tissue targets.     

C5aR activation in the absence of C5a: A new disease mechanism of autoimmune hemolytic anemia in mice

IgG Fc receptors (FcγRs) and the C5a anaphylatoxin receptor (C5aR) were identified as key regulators of type II autoimmune injury in mice. However, and with respect to C5aR, the relative importance of C5a for IgG autoantibody‐induced cellular destruction remained unclear. Using an experimental model of autoimmune hemolytic anemia (AIHA), we here report marked differences in the development of AIHA between mice lacking C5aR and C5‐deficient (Hc⁰) strain, indicating a limited role of C5 in this type of C5aR‐regulated disease. Ex‐vivo‐analyses of liver homogenates from anemic Hc⁰ mice demonstrate C5a‐independent C5aR activation, upregulation of FcγR expression and amplification of erythrophagocytosis by macrophages. As assessed by pharmacological inhibition studies, targeting of C5aR, but not of C5, is effective in treating experimental AIHA. Collectively, these results define a previously unrecognized disease mechanism of C5aR activation in AIHA that does not necessarily involve C5 and C5a.     

Aceclofenac spares cyclooxygenase 1 as a result of limited but sustained biotransformation to diclofenac

OBJECTIVE: The mechanism of action of aceclofenac is currently unclear. This study investigated whether biotransformation to metabolites (4'-hydroxy-aceclofenac, diclofenac, 4'-hydroxy-diclofenac) contributes to inhibitory effects on the cyclooxygenase (COX) isozymes in vitro and ex vivo. METHODS: In vitro investigations were performed with human whole blood and human blood monocytes. A randomized crossover study was performed in volunteers receiving 100 mg aceclofenac or a sustained-release resinate formulation of 75 mg diclofenac to assess the pharmacokinetics and the ex vivo inhibition of COX-1. RESULTS: In short-term in vitro assays, neither aceclofenac nor 4'-hydroxy-aceclofenac affected COX-1 or COX-2, whereas diclofenac and 4'-hydroxy-diclofenac inhibited both isoforms. In long-term in vitro assays, aceclofenac and 4'-hydroxy-aceclofenac suppressed both COX isoforms. However, this inhibition was paralleled by a conversion to diclofenac and 4'-hydroxy-diclofenac, respectively. Maximal plasma concentrations of diclofenac after oral administration of aceclofenac (0.39 micromol/L) or diclofenac (1.28 micromol/L) were sufficient for a greater than 97% inhibition of COX-2 (50% inhibitory concentration, 0.024 micromol/L) and a 46% (aceclofenac treatment) or 82% inhibition (diclofenac treatment) of COX-1 (50% inhibitory concentration, 0.43 micromol/L). Moreover, ex vivo COX-1-dependent thromboxane B(2) synthesis was inhibited significantly less by aceclofenac than by diclofenac. CONCLUSIONS: Inhibition of COX isozymes by aceclofenac requires conversion into diclofenac. Although 100 mg aceclofenac yielded diclofenac concentrations substantially lower than 75 mg diclofenac, these were sufficient for a sustained block of COX-2 but caused a minor and shorter inhibition of COX-1 than 75 mg diclofenac. In conclusion, both COX-1-sparing and COX-2-inhibitory actions of aceclofenac may rest in its limited but sustained biotransformation to diclofenac.