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×èòàòåëü Íåäóã.Ðó
Íå íàøëà ÿ ìûëî. Èäó íà ñïèä.ðó. Ïîìîãèòå ìíå.
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×èòàòåëü Íåäóã.Ðó
Äëÿ ÏÐÎÑÒÎ ÃÎÑÒÜ. Íåò ó òåáÿ âè÷, òåáå æå îòâåòèë äîêòîð, ÿ íå äóìàþ, ÷òî ýòî ñêðûâàþò îò ïàöèåíòîâ.
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×èòàòåëü Íåäóã.Ðó
Òàê ïåðâûé ðåçóëüòàò? ß åãî òîëüêî, ÷òî äîñòàëà. Ýòî îò ÷àñòíîãî Äîêà.
À íà 6 ìåñÿöåâ ÿ ó ó÷àñòêîâîãî ïðîâåðÿëàñü???? ×òî ýòî?
Íàãðóçêà? ß íå ïîíèìàþ. Î ÷åì ãîâîðÿò ýòè öèôðû? Ìåíÿ êîëáàñèëî ñèëüíî.
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Ñîîáùåíèå îò ïðîñòî
Òóò íàðîä êàê òî áîëåå â ïàíè÷åñêóþ àãðåññèþ âïàäàåò, Âû ëó÷øå ïî ëè÷êå, ìûëó, àñêå, ñêàéïó ïèøèòå.
À ôîáèòü íå íàäî, à òî íå óñíåòå.
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×èòàòåëü Íåäóã.Ðó
ß áëàãîäàðþ Âàñ. ß ñêèíóëà Âàì îäíî ñëîâî. ß íå ðåàãèðóþ íà ïî÷òó. Òÿæåëî. Åñëè äî óòðà äîæèâó. Çàâòðà ñìîãó îáñóäèòü. Ñåðäöå ñæàëî. Ñïîêîéíîé íî÷è.
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Endotoxin levels in the serum of normal healthy volunteers is less than 3 pg/ml (Obayashi et al. Clinica Chimica Acta 1985, 149:55-65). It has been reported that 0.5 ng/kg (7 pg/ml in a 70 kg adult) endotoxin produces granulocytosis of 200-300% within 4 hours in normal healthy volunteers (Wessels et al. Crit. Care Med. 1988 16:601-605). A slightly higher dose of endotoxin, 0.8 ng/kg (10 pg/ml) is pyrogenic. Levels greater than 20 pg/ml have been associated with septicemia (Zhang et al. J. Clin. Microbiol. 1994 32:416-422).
pg => pictogramm = 1/1000,000,000 kg
mcr => microgram = 1/1000,000 kg
ìêã íå èìååò íèêàêîãî ñìûñëà ó âàñ.
åñëè íà ñàìîì äåëå òàì ïã òî ñåïòèñåìèè ó âàñ íåò.
åñëè ýòî EU/ìë, ó âàñ âûñîêàÿ ýíäîòîêñèìèÿ.
Endotoxin plasma levels started to increase significantly after induction of anesthesia from 0.04 to 0.13 EU/ml. Peak values of 0.24 EU/ml were observed before the closure of the abdominal wall. Mesenteric lymph nodes obtained from 34 pts. after mobilization of the organ which should be resected were found positive for bacterial growth in 12 cases.
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http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
Relationship between gastro-intestinal complaints and endotoxaemia, cytokine release and the acute-phase reaction during and after a long-distance triathlon in highly trained men.
Jeukendrup AE, Vet-Joop K, Sturk A, Stegen JH, Senden J, Saris WH, Wagenmakers AJ.
Department of Human Biology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. A.E.Jeukendrup@bham.ac.uk
The aim of the present study was to establish whether gastro-intestinal (GI) complaints observed during and after ultra-endurance exercise are related to gut ischaemia-associated leakage of endotoxins [lipopolysaccharide (LPS)] into the circulation and associated cytokine production. Therefore we collected blood samples from 29 athletes before, immediately after, and 1, 2 and 16 h after a long-distance triathlon for measurement of LPS, tumour necrosis factor-alpha and interleukin-6 (IL-6). As the cytokine response would trigger an acute-phase response, characteristic variables of these responses were also measured, along with creatine kinase (CK) to obtain an indicator of muscle damage. There was a high incidence (93% of all participants) of GI symptoms; 45% reported severe complaints and 7% of the participants abandoned the race because of severe GI distress. Mild endotoxaemia (5-15 pg/ml) was evident in 68% of the athletes immediately after the race, as also indicated by a reduction in IgG anti-LPS levels. In addition, we observed production of IL-6 (27-fold increase immediately after the race), leading to an acute-phase response (20-fold increase in C-reactive protein and 12% decrease in pre-albumin 16 h after the race). The extent of endotoxaemia was not correlated with the GI complaints or the IL-6 response, but did show a correlation with the elevation in C-reactive protein (r(s) 0.389; P=0.037). Creatine kinase levels were increased significantly immediately post-race, and increased further in the follow-up period. Creatine kinase levels did not correlate with those of either IL-6 or C-reactive protein. It is therefore concluded that LPS does enter the circulation after ultra-endurance exercise and may, together with muscle damage, be responsible for the increased cytokine response and hence GI complaints in these athletes.
Ïî êîððåëÿöèÿì ëþáîïûòíàÿ ñòàòüÿ. Ñòðåññ âûçûâàåò ýíäîòîêñèíåìèþ, êîòîðàÿ â ñâîþ î÷åðåäü ïðîâîöèðóåò ãàñòðî-êèøå÷íûå ñèìïòîìû.
Óðîâåíü ñðåäíåé ýíäîòîêñèíåìèè 5-15 pg/ml.
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We estimate that a single cystic kidney in an adult male (3-5 kg kidney weight of which 33% is cyst fluid) contains 648 to 1,080 EU/kidney or about two lethal doses of endotoxin per kidney. Unexplained fever and flank pain in PKD patients have been attributed to release of IL-1 from rupture or hemorrhage of cysts (27). On the bases of the high levels of endotoxin observed in this study and the high sensitivity of humans to endotoxin, we propose that the release of endotoxin from the cyst into the peritoneum or blood may be an important initiator of a cascade of biologic events after leakage or rupture of renal cysts.
Ïî íàøåé îöåíêå îäíà öèñòè÷íàÿ ïî÷êà â ìóæ÷èíå (3-5 êã âåñ ïî÷êè èç êîòîðîé 33% - ýòî êèñòîçíàÿ æèäêîñòü) ñîäåðæèò 648 äî 1080 EU íà ïî÷êó èëè îêîëî äâóõ ëåòàëüíûõ äîç ýíäîòîêñèíà íà ïî÷êó. Íåîáúÿñíèìàÿ ëèõîðàäêà è áîëü â áîêó â ÏÊÁ áîëüíûõ äî ýòîãî îòíîñèëàñü ê IL-1 èç ðàçðûâîâ èëè ãåìîðàæà êèñò. Îñíîâûâàÿñü íà âûñîêèõ óðîâíÿõ ýíäîòîêñèíà íàáëþäàåìûõ â èññëåäîâàíèè è ÷óâñòâèòåëüíîñòè ëþäåé êê ýíäîòîêñèíó, âû ïðåäëàãàåì òåîðèþ ÷òî âûõîä ýíäîòîêñèíà èç êèñòû â ïåðèòîíèé èëè êðîâü ìîæåò áûòü âàæíûì èíèöèàòîðîì â êàñêàäå áèîëîãè÷åñêèõ ïðîèøåñòâèé ïîñëå ïîäòåêàíèÿ èëè ðàçðûâà ïî÷å÷íûõ êèñò.
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Ò.å. ëåòàëüíàÿ äîçà ýíäîòîêñèíà - ýòî ïðèìåðíî 300 EU (áåç ìë). Ó æåíùèíû êðîâè ïðèìåðíî ñêàæåì 10 ëèòðîâ. Ò.å. ïðè êîíöåíòðàöèè 1,25 EU/ml â êðîâè ñîäåðæèòüñÿ îêîëî 12,500 EU ÷òî áîëåå 40 ðàç âûøå äåòàëüíîé äîçû òîêñèíà.
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Ó íåìêè â ñïèíîìîçãîâîé æèäêîñòè áûëà êîíöåíòðàöèÿ 6600 pg/ml.
îáúåì â ëèòðàõ åå ñïèíîìîçãîâîé æèäêîñòè ðàâåí 125 ìë.
Âñåãî (íåòòî): 825,000 ïã. (ßÄ)
Óðîâåíü íîðìàëüíûé â ïëàçìå 4-5 pgml.
Âñåãî (íåòòî) 15,000 ïã
ng = 1000 pg = 12 EU
5 pg/ml = 0,06EU/ml x 3000 ==> 180 EU
15 pg = 0,18 EU x 3000 ===> 540 EU
1,25 EU/ml = 102 pgml x 3000 4750 EU 305,000 pg
íîðìàëüíûé óðîâåíü â ïëàçìå 5pg/ml 180EU. 0,06 EU/ml â ñðåäíåì 3 l.
ñåïòèñåìèÿ ñðåäíÿÿ 5-15 pgml 540EU 0,18 EU/ml
ïðè íîðìàëüíîì 180 åùå 350 ==> 530~540 ==> 0,2 EU/ml ñåïòè÷åñêèé øîê.
ò.å. Îëüãà èëè ó âàñ ñåïòèñåìèè íåò èëè ëåòàëüíûé ïîêàçàòåëü ïðåâûøåí â 6 ðàç. íåîáõîäèìî åäèíèöû óòî÷íèòü.
1,25 EU/ml ===> Í È Ê À Ê È Õ Ø Ó Ò Î Ê.
Èíåñ ïèñàëà ÷òî è 1,25 pgml óæå ìîæåò êîëáàñèòü. (îíà íå â òåìå çäåñü, íî òåì íå ìåíåå, ïîñî÷óâñòâîâàëà íàâåðíîå.) Óðîâíè ðàçëè÷àþòñÿ â 90 ðàç ïðèìåðíî.
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Êèðèëë, òû òîëüêî ó÷òè ÷òî â 6 ðàç ó Îëüãè áûòü ïðåâûøåí íå ìîæåò, ò.ê. íîðìàëüíûå çíà÷åíèÿ äî 1, à ó íåå 1.25
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óãó, äî 1 pg/ml,- îäíîçíà÷íî.
1,25 EU/ml ===> 102 pg/ml; èç ðàñ÷åòà 1ng = 12 EU, 3L ïëàçìû.
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At the same time point 50 out of 56 pts. had increased endotoxin plasma levels (0.19 EU/ml).
 òîæå âðåìÿ 50 èç 56 ïàöèåíòîâ èìåëè ïîâûøåííûå óðîâíè ýíäîòîêñèíà â ïëàçìå 0.19 EU/ml. [ðå÷ü î ñåïñèñå ïðè àáäîìèíàëüíîé õèðóðãèè - Ñ.].
http://www.ssat.com/cgi-bin/abstract...i?affiliation=
D Berger, E Bolke, M Seidelmann, HG Beger. Department of General Surgery, University of Ulm, Germany.
0.19 EU/ml. - ïîâûøåííîå, â ñðåäíåì öèôðà 0,05 EU.
Íèêòî íå ãîâîðèò ÷òî ïðè 1,25 EU/ml ÷åëîâåê ñðàçó èäåò êèëåì ââðåõ.
Òîëüêî ïðè ðåçêîì ââåäåíèè âíóòðèâåííîì ýíäîòîêñèíà.
ß áû èíòîêñèêàöèþ ñðàâíèë 1 EU/ml - ñ 1 ë. âîäêè.
íîðìàëüíûå ëþäè èëè âûïèâàþò 0,05 EU/ml - 50 ã
èëè ñòàêàí 0,19 EU/ml èëè òðåçâûå ñ ôîíîì â 0,01 EU/ml.
À äëÿ òåõ êòî îòñûëàåò "ê ãîìåîïàòàì", ïîëàãàþ 1 ë. - ÍÅ ÏÐÅÄÅË.