Laparoendoscopic Single-site Plus 1-port Donor Nephrectomy: Division of Roles to Shorten Warm Ischemic Time.

BACKGROUND: In this study we present our new surgical procedure, laparoendoscopic single-site surgery plus 1 for donor nephrectomy (LESS+1-DN), which shortens warm ischemic time (WIT) and improves surgical outcomes. METHODS: From January 2013 to February 2017, 15 patients who underwent LESS-DN and 41 patients who underwent LESS+1-DN at our institution were evaluated retrospectively. Patients were divided into 3 groups: group A, 15 cases of LESS-DN; group B, the first 15 patients who underwent LESS+1-DN; and group C, 26 patients who underwent subsequent LESS+1-DN. To reduce WIT, we clearly defined the roles of the surgeon and first assistant in the 26 subsequent LESS+1-DN cases. The surgeon dissected the renal pedicle and harvested the kidney graft using a recovery bag and the first assistant held the recovery bag. RESULTS: The mean operative time in group C (213.7 minutes) was significantly shorter than that in groups A (253.3 minutes) and B (253.8 minutes). The WIT in group C (195.2 seconds) was significantly shorter than that in groups A (389.8 seconds) and B (313.2 seconds). Open conversion was required in 1 case in group A. None of the donors required conversion to open surgery and no perioperative complications occurred in groups B and C. Linear regression analysis of the LESS+1-DN operative times and consecutive case numbers demonstrated a shallow learning curve (R2 = 0.392, P < .05). CONCLUSION: Our new procedure that divides the roles of the operator and the first assistant contributed significantly to a shortening of WIT. Dividing roles can facilitate a safer laparoscopic donor nephrectomy.

Early progression stage of malignancy as revealed by immunohistochemical demonstration of DNA instability; I, Human gastric adenomas.

The degree of DNA-instability as revealed by the immunohistochemical staining with monoclonal anti-single-stranded DNA antibody after acid hydrolysis (DNA-instability test) was used as the marker of malignancy. This was applied to human gastric regenerative epithelium in chronic peptic ulcer (5 cases), adenoma (35 cases), and well differentiated tubular adenocarcinoma (5 cases). Proliferative activity was evaluated by proliferating cell nuclear antigen (PCNA) immunohistochemistry, and the quantitative analyses of the mean number and mean area of silver-stained nucleolar organizer regions (AgNORs) per one nucleus were performed for all these cases. All cancers and adenomas were positively stained by the DNA-instability test diffusely, indicating the malignant character of the latter from the view point of DNA-instability, in contrast to the negative stainability of all regenerative epithelium. The percent number of PCNA-positive cells and mean number and mean area of AgNORs tended to be larger in adenoma and cancer than in regenerative epithelium, although the differences were not usually statistically significant. Supporting the malignant character of adenoma, single cell necroses and abnormal mitoses were almost always present in the lesion. In conclusion, all adenoma lesions were regarded as malignant in nature, namely, in-situ carcinoma, existing at an early stage of progression of malignancy.

[Cholera epidemics in Kanagawa].

In 1822 cholera first arrived in Japan, but it did not reach Edo, which is the old name of Tokyo, nor Kanagawa, a prefecture located next to Tokyo. During a second epidemic in 1858, 30,000 or so Japanese died and Kanagawa had a heavy toll. Cholera raged in Japan in 1877, 1879, 1882, 1886, 1890, 1891 and 1895. In 1877, an American doctor named D.B. Simmons was working at Juzen Hospital (the previous hospital of Yokohama Medical College) in the Noge area in Yokohama, Kanagawa. He and his team tried to cure cholera patients by disinfecting the patients and their wastes with carbolic acid or phenol. They knew that isolating the patients was a good way to prevent the epidemic. As there was no hospital for infectious diseases in Kanagawa, they hurriedly built a small temporary hospital near Juzen Hospital and named it Ota Isolation Hospital, where cholera patients were sent and treated. In 1879 as people suffered again from an epidemic Ota Hospital was replaced by Izumicho Isolation Hospital, which became a hospital for infectious diseases two decades later in 1900 and was called Yokohama Manji Hospital. Manji means to cure all. Wilhermus Hubertus van der Heyden, a Dutch doctor, worked for this hospital. The first regulation of cholera prevention in Japan was issued by the Bureau of Health of the Ministry of Internal Affairs in 1879. ...

A role for Ca2+ in mediating hormone-induced biphasic pepsinogen secretion from the chief cell determined by luminescent and fluorescent probes and X-ray microprobe.

In isolated chief cells from the guinea pig, cholecystokinin (10 nM) and a high concentration of ionomycin each caused a biphasic pattern of pepsinogen secretion. The initial fast response to cholecystokinin was not dependent on medium Ca2+ ans was mimicked by low concentration of ionomycin (100 nM). Inositol 1,4,5-trisphosphate caused a similar fast release from permeabilized cells. The slow component of release was dependent on medium Ca2+, however, and was mimicked by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) (100 nM) or the diacylglycerol analogue 1-oleoyl-2-acetylglycerol (OAG) (100 microM). Ionomycin (100 nM) and TPA (and/or OAG), when applied together, reproduced the biphasic pattern of pepsinogen secretion, suggesting that the signalling pathways utilized by both types of agonist contribute to the response evoked by cholecystokinin-hormone stimulation. Both fura-2 and aequorin were used to monitor changes of intracellular Ca2+. Three pathways were found to contribute to the Ca2+ transient. A rapid release of Ca2+ from intracellular store(s), a rapid Ca2+ entry from the extracellular space, and a more sustained Ca2+ entry from the extracellular space. Cholecystokinin induced a rapid increase in cytoplasmic Ca2+ ([Ca2+]i) as estimated with fura-2 and aequorin. This rise was reduced but not abolished upon removal of extracellular Ca2+, suggesting that both Ca2+ entry from the extracellular space and Ca2+ mobilization from the intracellular store(s) contribute to the initial, fast component of the Ca2+ transient. A second, more sustained component of the Ca2+ transient induced by cholecystokinin was abolished by lanthanum. TPA and OAG induced a biphasic Ca2+ transient that could be detected only with aequorin. The late, sustained component of this response was again abolished by lanthanum as well as by removal of extracellular Ca2+. It appears that the late component of the Ca2+ transient is dependent on Ca2+ influx from the extracellular space and is too localized to be detected by fura-2. Prestimulation of cells with TPA or OAG prevented the aequorin transient caused by cholecystokinin and vice versa, suggesting that TPA, OAG and cholecystokinin activate the same pathways of Ca2+ entry into the cytosol from the intracellular store(s) or the extracellular space. The stimulation-sensitive Ca2+ pool was examined with electron probe X-ray microanalysis. It appears to be restricted to an area enriched in secretory granules or peripheral endoplasmic reticulum just beneath the apical plasma membrane and in close association with the microtubular-microfilamentous system.(ABSTRACT TRUNCATED AT 400 WORDS)

Intracellular Ca2+ shift and signal transduction from the tubulovesicular portion of gastric parietal cells during gastrin stimulation or Ca2+ ionophore treatment: comparison between luminescent and fluorescent probes, and electron probe X-ray microanalyzer.

In gastrin-stimulated, aequorin-loaded parietal cells from guinea pig gastric mucosa, a rapid but transient increase in the cytosolic free Ca2+ concentration ([Ca2+]i), owing to Ca2+ released from the store(s), and a more prolonged Ca2+ entry from outside the cells were observed. However, there was a little increase in [Ca2+]i when similar measurements were assessed by quin 2 or fura-2 in physiological saline. However, depletion or elimination of Na+ from the incubation medium caused a significant increase in the [Ca2+]; response to gastrin as measured by quin 2. These findings suggest that aequorin and quin 2 (or fura-2) provide information about different aspects of Ca2+ homeostasis and that there is an inhomogeneity of [Ca2+]i in the cytoplasm during gastrin stimulation. By the gastrin stimulation, the intracellular Ca2+ gradients were shifted from the unidentified portion(s) to the restricted apical cytoplasm, as determined by electron probe X-ray microanalysis. Therefore, localization and identification of the source of intracellular Ca2+ as a pool were determined by an X-ray microanalyzer. In the resting state, the tubulovesicle had high Ca2+ concentration compared with the level in the apical cytoplasm. Cells treated with the Ca2+ ionophore ionomycin had a decreased tubulovesicular Ca2+ level, followed by a reciprocal increase in area of the canalicular membrane. The secretory canaliculus in stimulated cells had lower Ca2+ or higher K+ and Cl- concentrations than that of tubulovesicles or cytoplasm in the resting state, respectively. These findings suggest that the Ca2+ pool of the parietal cell is in the tubulovesicles and (or) luminal cell membrane and that the Ca2+ released from the store(s) may mediate a flow of K+ or Cl- into the secretory canaliculus.