Hand-assisted retroperitoneoscopic living donor nephrectomy superior to laparoscopic nephrectomy.
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Biomedical subjects
Publications and source records attributed to P Lindström.
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AIM: Oliguria is seen during elevated intraperitoneal pressure, but the physiological mechanisms are not yet clarified. The purpose of the present study was to investigate the changes in renal function, cardiac output and distribution of systemic blood flow (BF) that occur in connection with an elevation of intra-abdominal pressure (IAP) in a rat model by isotope-labelled microsphere technique. METHODS: A 5 or 10 mmHg IAP was created by CO2 insufflation and maintained for 90 min in anaesthetized and mechanically ventilated rats. Rats with normal IAP served as controls. Blood flow and cardiac output measurements by injection of isotope-labelled microspheres were conducted at three time points. Acid-base balance, urine output, glomerular filtration rate (GFR) and urinary excretion products were also followed. RESULTS: Glomerular filtration rate decreased [0.7-0.1 mL min(-1) g(-1) kidney weight (KW)] with elevated IAP, as did urine output (8.5-0.6 microL min(-1) g(-1) KW). Dramatic decreases were seen in renal excretion of sodium (by 97%), potassium (by 94%) and osmotic active substances (by 93%). Cardiac output was diminished by 54% at 5 mmHg and by 65% at 10 mmHg intraperitoneal pressure and systemic vascular resistance (SVR) was elevated threefold. CONCLUSION: Cardiac output, measured by microsphere technique, decreased during elevated intraperitoneal pressure by CO2 in anaesthetized rats, while SVR was elevated and renal excretory functions were decreased to a large extent.
To investigate the hormonal and cellular selectivity of the prandial glucose regulators, we have undertaken a series of experiments, in which we characterised the effects of repaglinide and nateglinide on ATP-sensitive potassium ion (KATP) channel activity, membrane potential and exocytosis in rat pancreatic alpha-cells and somatotrophs. We found a pharmacological dissociation between the actions on KATP channels and exocytosis and suggest that compounds that, unlike repaglinide, have direct stimulatory effects on exocytosis in somatotrophs and alpha- and beta-cells, such as sulphonylureas and nateglinide, may have a clinically undesirable general stimulatory effect on cells within the endocrine system.
BACKGROUND: Hand-assisted laparoscopy (HALS) was introduced to increase the safety of living donor nephrectomies. Herein we evaluate the first HALS living donor nephrectomies performed at our center. METHODS: Traditional laparoscopic nephrectomies (TLS) (n = 11) and HALS nephrectomies (n = 11) were included in the study. One patient from the TLS group was excluded because the operation was converted to open nephrectomy. We compared the operating times (OT) and warm ischemia times (WIT) for the two procedures and calculated the operating costs. RESULTS: Mean OT was 270 min in the TLS group and 197 min in the HALS group; thus, there was, a significant reduction of 27% with HALS. WIT was 297 sec for the TLS group and 214 sec for the HALS group, for a reduction of 28%. Costs were also lowered for HALS. CONCLUSION: In addition to shortening both OT and WIT, HALS enhances the safety margin of the procedure, especially during trocar placement. It is further helpful in preventing torsion of the kidney and controlling potential bleedings, as well as during vascular stapling and kidney removal.
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Jurkat E6-1 cells obtained from three different sources were compared with respect to intracellular calcium response to a 50 Hz, 0.15 mT, magnetic field, to treatment with poly-L-lysine and to protein expression at the cell surface. The fura-2 single cell measurements were a replication study performed by three members of our group. The cells responded to the applied magnetic fields, although the percentage of responding cells was lower than in earlier studies. The geomagnetic field was backed off without changing the outcome of the intracellular calcium measurements. Fluorometric analyses showed no difference between the E6-1 cells obtained from three sources with respect to the expression of cell surface marker molecules. The addition of the cell adhesive peptide, poly-L-lysine, did not itself cause any effects on the intracellular calcium concentration.
These experiments tested the effect of 10 to 30 mg, citalopram/kg body weight on food intake, weight increase, and blood glucose levels in young obese hyperglycemic mice (Umeå ob/ob). A leptin defect in ob/ob mice results in hyperphagia, hyperglycemia, and increased body weight compared with normal mice. Citalopram had no effect on weight increase in ob/ob mice aged 3 to 10 weeks, when the weight increase is most rapid. Citalopram reduced the weight increase at the age 10 to 19 weeks. Food intake reaches a maximum at age 7 to 10 weeks and then decreases. The reduction was more rapid in citalopram-treated mice. The weight of feces paralleled the food intake. Citalopram treatment had no effect on serum insulin levels in 15-week-old mice. Blood sugar values in fed mice reached a peak at age 7 weeks (21.7 +/- 1.7 mmol/L in controls and 22.3 +/- 1 mmol/L in citalopram-treated mice). After that, blood sugar values decreased. The decrease was more pronounced in citalopram-treated mice (P < .01 compared with controls). Blood glucose levels were lower at ages 12 to 15 weeks in female ob/ob control mice (13.6 +/- 2.5 mmol/L v 19.0 +/- 0.6 mmol/L in male control mice; P < .05). The effect of citalopram was the same in male and female mice. There was a close correlation between accumulated food intake and blood glucose values in individual animals. At age 3 to 10 weeks, ob/ob mice have a high beta-cell proliferation rate, and they have large islets of Langerhans. This was not affected by citalopram treatment. Our findings show that the serotonergic system plays a role as a regulator of food intake over shorter periods, and this is also true in the absence of leptin.
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Retrospective analysis and comparison of a small series of 12 laparoscopic live donor nephrectomy (LapLDN) procedures with 15 open live donor nephrectomies, all 27 performed in 1998, showed operating time to be significantly longer but sick leave shorter and hospital stay somewhat shorter in the LapLDN subgroup. One patient in the open procedure subgroup developed herniation and scar discomfort, and in one LapLDN procedure severe bleeding necessitated conversion to open nephrectomy. All kidneys in both subgroups manifested immediate resumption of function after transplantation. Though the LapLDN procedure has yet to be satisfactorily evaluated, the present findings were predominantly in its favour.
Pancreatic islets from obese hyperglycemic mice are large and contain a high proportion of normally functioning beta-cells. We have previously shown that young obese mice have an elevated beta-cell proliferation rate at 3 weeks of age. We now wanted to investigate possible factors involved in the initiation of islet growth, including blood glucose, C peptide, glucagon-like peptide-1, vasoactive intestinal polypeptide, and L-5-hydroxytryptophan. We found that the increased beta-cell proliferation on day 20 precedes the rise in blood glucose by 2 days. The islet cell proliferation, measured as the 5-bromo-2'-deoxyuridine labeling index, in 20-day-old lean mice, was enhanced in a dose-dependent manner when glucagon-like peptide-1 or C peptide was injected s.c. for 2 days. L-5-Hydroxytryptophan inhibited the proliferation. C Peptide also increased the islet cell labeling index during islet culture. We conclude that in addition to the effect of glucose, islet proliferation can be triggered by other factors involved in the physiological regulation of increased insulin release. Stimulation of islet proliferation may be related to the actual release of insulin, and C peptide may function as a mediator of such responses.
Obese hyperglycemic mice have large pancreatic islets and high levels of serum insulin and blood glucose. Vagotomy was performed on 3-wk-old animals to investigate the role of gut cholinergic innervation in young Umea ob/ob mice. After vagotomy, obesity and hyperglycemia are dissociated. Weight increase in obese vagotomized mice was lower than in sham-operated controls during the 1st wk postoperatively but not thereafter. Blood glucose was lower up to 5 mo after vagotomy, but vagotomized mice showed reduced glucose tolerance. Islet cell proliferation rate was reduced 2 and 3 wk but not 5 mo after vagotomy. After 5 mo, islet volume was smaller in vagotomized mice. Serum insulin levels were the same in vagotomized animals as in sham-operated controls. The effects of reduced cholinergic innervation are probably caused both by direct effects of denervation and by lowered metabolic demand.
OBJECTIVE: In Sweden there has been a continuous decrease in the autopsy rate during the last 15-20 years. The autopsy rate in the city of Malmö has declined from 81% in 1984 to 34% in 1993. The intention of this study was to improve our understanding of the causes of the decline, and to assess its consequences with regard to cause of death surveillance and case retrieval in epidemiological and clinical research. DESIGN: A retrospective study. SETTING: The University Hospital in Malmö, a city in southern Sweden with 230000 inhabitants. SUBJECTS: All deceased in 1984 (2900) and 1993 (3198). Cancer incidence 1984 and 1993. MAIN OUTCOME MEASURES: Changes in autopsy rate in relation to age, sex, place of death and cause of death 1984 and 1993. Changes in the distribution of underlying causes of death in cases submitted and not submitted for a post mortem 1984 and 1993. Changes in cancer incidence and the number of incidentally-detected new tumours 1984 and 1993. RESULTS: Patients who died in nursing homes were less often sent for a post mortem than were patients who died at the hospital. From 1984 to 1993 the percentage of people dying in nursing homes increased from 1 to 29%. Care of the elderly has been reorganized, and the number of terminally ill patients who die in nursing homes has increased during the last 20 years in Sweden. This shift in place of death seems to be the single major explanation of the declining autopsy rate in Malmö. The overall autopsy rate in 1993 remained, however, lower than it was in 1984 when a shift in place of death was taken into account. During the period of study there was a decline in the autopsy rate at all departments within the hospital. The distribution of underlying causes of death according to the death certificates was similar in 1984 and in 1993. However, in cases not submitted for autopsy in 1993 there were greater proportions dying from pulmonary and circulatory diseases, respectively, than there were in 1984. The lower autopsy rate in 1993 was for several cancer sites also associated with a reduced number of new cancer cases. The percentage of tumours incidentally detected at autopsy went down in men from 40 to 19% and in women from 39 to 17%. CONCLUSION: Patients submitted for autopsy represented, with regard to age, sex, cause and place of death, a selected group of all deceased. The declining autopsy rate was associated with a difference in the distribution of underlying cause of death and of the incidence of cancer. It is concluded that the changes in the autopsy rate have to be taken into account in studies dealing with time trends of causes of death and incidence of cancer.
OBJECTIVES: To determine if the recovery of nerve function after ischaemic block is impaired in patients with diabetes mellitus relative to healthy controls. METHODS: Median nerve impulse conduction and vibratory thresholds in the same innervation territory were studied in patients with diabetes mellitus (n = 16) and age matched controls (n = 10) during and after 30 minutes of cuffing of the forearm. RESULTS: Cuffing caused a 50% reduction of the compound nerve action potential (CNAP) after 21.9 (SEM 1.6) minutes in patients with diabetes mellitus and after 10.6 (0.7) minutes in controls. After release of the cuff the half life for CNAP recovery was 5.13 (0.45) minutes in patients with diabetes mellitus and <1 minute in controls. At seven minutes after release of the cuff CNAP was fully restored in the controls whereas in patients with diabetes mellitus CNAP had only reached 75.1 (4.1)% of its original amplitude. After onset of ischaemia it took 14.6 (1.9) minutes in patients with diabetes mellitus before the vibratory threshold was doubled, whereas this took 5.8 (0.8) minutes in controls. After release of the cuff half time for recovery of vibratory threshold was 8.8 (1.0) minutes in patients with diabetes mellitus and 2.6 (0.3) minutes in controls. Ten minutes after the cuff was released the threshold was still raised (2.0 (0.3)-fold) in the diabetes mellitus group, whereas it was normalised in controls. Among patients with diabetes mellitus the impaired recovery correlated with older age, higher HbA1c, and signs of neuropathy, but not with blood glucose. CONCLUSION: After ischaemia there is a delayed recovery of nerve conduction and the vibratory sensibility in patients with diabetes mellitus. Impaired recovery after ischaemic insults may contribute to the high frequency of entrapment neuropathy in patients with diabetes mellitus.
Hypoglycemic sulfonylureas represent a group of clinically useful antidiabetic compounds that stimulate insulin secretion from pancreatic beta cells. The molecular mechanisms involved are not fully understood but are believed to involve inhibition of potassium channels sensitive to adenosine triphosphate (KATP channels) in the beta cell membrane, causing membrane depolarization, calcium influx, and activation of the secretory machinery. In addition to these effects, sulfonylureas also promoted exocytosis by direct interaction with the secretory machinery not involving closure of the plasma membrane KATP channels. This effect was dependent on protein kinase C (PKC) and was observed at therapeutic concentrations of sulfonylureas, which suggests that it contributes to their hypoglycemic action in diabetics.
BACKGROUND: In normal prostate, TGF-beta 1 is associated to castration induced apoptosis. Combined castration and estrogen treatment, but not castration alone, induces apoptosis in the Dunning R3327 PAP adenocarcinoma. METHODS: TGF-beta 1 expression in rat ventral prostate (VP) and Dunning R3327 PAP tumor was studied after castration and estrogen treatment, using competitive RT-PCR, in situ hybridization and immunohistochemistry. RESULTS: TGF-beta 1 mRNA level was 6 times higher in the tumor than in the VP. Combined castration and estrogen treatment increased TGF-beta 1 mRNA levels in the tumor from day 3, while castration did not. The TGF-beta 1 expression was located in the epithelial cells. CONCLUSIONS: The Dunning R3327 PAP tumor contains high levels of TGF-beta 1, which are further increased by combined castration and estrogen treatment. However, since this increase is not apparent until day 3, TGF-beta 1 probably does not contribute to the known induction of apoptosis in the tumor at day 1 after combined castration and estrogen treatment.
Enriched fractions of heavily granulated (type II) and sparsely granulated (type I) somatotrophs have been prepared from male Sprague-Dawley rats by Percoll density gradient centrifugation in two steps. After 3 days of culture, basal GH release was 0.116 +/- 0.024 (n = 30) and 0.223 +/- 0.034 ng GH/microgram protein-min (n = 34) in type I and type II cells, respectively (P < 0.05). GH-releasing hormone (GHRH; 0.01-10 nM) stimulated GH release in type II cells, whereas type I cells only responded to higher doses of GHRH (1 and 10 nM). The dynamics of GH release were similar in the two cell types. Type II cells released more GH in absolute values, which may reflect the higher GH content in these cells. The somatostatin analog octreotide (100 pM) reduced basal GH release by 63% in type I cells, but by only 17% in type II cells. Octreotide also had a slightly greater effect on GHRH-induced GH release in type I cells. Both cell types responded to 100 nM GH-releasing peptide-6. We conclude that both type I and type II somatotrophs contribute to GH release, but type II cells are more sensitive to and release more GH when stimulated with GHRH. The role of type I cells may be to boost the initial secretory response at the onset of physiological pulses.