I-Atherossteosis iyimbangela ehamba phambili yesifo senhliziyo nemithambo yegazi, ehlala ingumholi emhlabeni wonke ekufeni.I-Insulin-like growth factor I (IGF1) iboniswe ukunciphisa izehlakalo zenhliziyo nemithambo yegazi.Ukuphathwa kwe-IGF1 kunciphisa ukuqina kwe-atherosclerosis kanye nokunciphisa ama-plaque macrophage ku-ApoE-deficient (Apoe- /-) amagundane adla ukudla okunamafutha amaningi.Imiphumela yethu yangaphambilini ye-in vitro iphakamisa ukuthi ama-macrophages adlala indima enkulu ekulamuleni imiphumela ye-IGF1 kuma-atherosclerotic plaques, kodwa indlela eqondile ayikacaci ngayo. ukuvimbela i-atherosclerosis.
Ngemva kokuzalanisa inoveli ye-macrophage-specific IGF1-overexpressing transgenic amagundane ku-Apoe-/- background (MF-IGF1 amagundane), sahlola umthwalo we-atherosclerotic plaque, ukuzinza, nokuqashwa kwama-monocyte. ukudla okunamafutha izinyanga ezintathu.Siphinde sahlola i-cholesterol efflux kanye nokwakheka kwamangqamuzana egwebu ku-vivo kanye ne-in vitro.
I-Macrophage IGF1 overexpression yehlise umthwalo we-plaque ngo-30%, yehlise ama-plaque macrophages ngo-47%, nezici ezithuthukisiwe ezizinzisa i-phenotype ye-plaque.Ukuqashwa kwama-Monocyte kwehliswe ngo-70% kumagundane e-MF-IGF1 futhi kuhlotshaniswa nokunciphisa okungu-27% kokujikeleza kwe-CXC. i-chemokine ligand 12 (CXCL12) .Amazinga amaprotheni e-CXCL12 ancishisiwe kuma-plaque kanye nama-macrophage e-peritoneal ku-MF-IGF1 amagundane.In vitro, i-IGF1 ivimbe ngokuphelele i-oxidized low-density lipoprotein (oxLDL) -ukwanda okuncike ekubhalweni kabusha kwe-PCCL12 mRNA% (9%). <0.01), kanye nokwelashwa kwe-IGF1 kunciphise amaprotheni e-CXCL12 (ukunciphisa okungu-56%, i-P <0.001).
I-CXCL12 yehlisa ukuvezwa kwe-ATP-binding cassette transporter A1 (ABCA1), isithuthi se-cholesterol esibalulekile esilamula i-cholesterol efflux evela kuma-macrophages.Sithole ukukhuphuka okuphindwe kabili kumazinga amaprotheni we-ABCA1 kuma-macrophage e-peritoneal ahlukaniswe namagundane e-MF-IGF1.Silinganise izinguquko ku-cholesterol efflux ngokulayisha ama-macrophages e-peritoneal nge-oxLDL futhi sathola ukwanda kwe-42% ku-efflux kumagundane e-MF-IGF1.Siphinde sathola ukwanda kwe-27% kwe-cholesterol efflux kumaseli we-THP-1 aphathwa nge-IGF1 (100 ng / mL) nge-apolipoprotein AI njenge-cholesterol receptor.
Imiphumela yethu ibonisa ukuthi i-macrophage IGF1 inciphisa i-atherosclerosis futhi inciphisa i-CXCL12, i-chemokine esanda kuhileleka ekuqhubekeleni kwe-atherosclerosis.IGF1 ingase inciphise i-CXCL12 ngokunciphisa ukuqashwa kwe-monocyte nokwandisa i-ABCA1, ngaleyo ndlela isebenzisa umphumela wayo we-atheroprotective, ngaleyo ndlela ikhulise umthamo we-cholesterol efflux.
Ukuguqulwa kwezakhi zofuzo ze-TTR (rs76992529; Val122Ile) kubonakala kuphela kubantu bokhokho base-Afrika (imvamisa yesibalo sabantu: 3-4%) okuholela ekugoqweni okungalungile kwe-tetrameric transthyretin complex, etholakala ku-hereditary transthyretin amyloidosis.I-Degeneration (hATTR) iqoqana njenge-extracellular amyloid fibrils.Ukulinganisa umthelela walokhu okuhlukile kwe-amyloidogenic TTR engozini yokwehluleka kwenhliziyo (HF) kanye nokufa okuyimbangela yonke eqenjini elikhulu, elihluke ngokwezindawo labantu base-Afrika baseMelika kunganikeza ukuqonda ngokubaluleka komtholampilo kwalokhu kwehluka. .Sihlole ababambiqhaza abansundu ocwaningweni lwe-Geographic and Racially Different Couses of Stroke (REGARDS) ukuze sihlole ukuhlotshaniswa kokuguqulwa kwe-TTR Val122Ile ne-HF kanye nokufa okuyimbangela.
Sihlole ababambiqhaza ababikiwe baseMelika abansundu ocwaningweni lwe-REGARDS ngaphandle kwe-HF ekuqaleni.Ukuhlehla kwe-Poisson kwasetshenziselwa ukulinganisa izehlakalo zokwehluleka kwenhliziyo kanye nokufa okuyimbangela yazo zonke.Sisebenzise imodeli ye-Cox regression eguquliwe eminingi ye-accounting ye-demographic, Clinical and social izici, kanye nezabo zofuzo zase-Afrika zokuhlola ubungozi be-HF kanye nokufa kwembangela yazo zonke izinhlobo kubantu abanofuzo oluhlukile lwe-TTR Val122Ile uma kuqhathaniswa nalabo abangenakho okuhlukile.
Phakathi kwabahlanganyeli abamnyama abangu-7,514 (iminyaka emaphakathi: iminyaka engu-64; 61% abesifazane), imvamisa yabantu yokuhluka kwe-TTR Val122Ile kwaba ngu-3.1% (abathwali abangu-232; 7,282 abangathwali). (95% CI: 11.5-21.9) phakathi kwezinkampani zenethiwekhi ezihlukile kanye ne-7.2 (95% CI: 6.6-7.9) phakathi kwezinkampani ezingathwali ezihlukile.Izinkampani zenethiwekhi ezihlukile ze-Val122Ile zibe nengozi enkulu yokuthuthukisa i-HF uma kuqhathaniswa nabangewona abathwali (HR: 2.46 [95% CI) : 1.72–3.53]; P<0.0001).Izehlakalo zokufa kwembangela yonke (iminyaka eyi-1000 yomuntu ngamunye) zazingu-41.5 (95% CI: 34.6-49.7) phakathi kwezinkampani zenethiwekhi ezihlukile kanye ne-33.9 (95% CI: 32.7)-3 phakathi kwezinkampani ezingezona zenethiwekhi ezihlukile.Izinkampani zenethiwekhi ezihlukile ze-Val122Ile zibe nengozi enkulu yokufa kwembangela yonke uma kuqhathaniswa nabangathwali (HR: 1.44 [95% CI: 1.18-1.76]; P=0.0004).Isimo senethiwekhi esihlukile se-TTR nobulili abuzange ukusebenzisana ne-HF kanye nemiphumela yokufa kwezimbangela zonke.
Eqeqebeni elikhulu labantu baseMelika abansundu, sibonisa ukuthi ukuguqulwa kwe-amyloid Val122Ile kufuzo lwe-TTR kuhlotshaniswa nengozi ephakeme ephindwe izikhathi ezingu-2.5 ye-HF kanye nengozi ephakeme ecishe ibe ngu-40% yokufa kwembangela. Ngokufika kwenqwaba ye-hATTR Izindlela zokwelapha, ukuba khona kokuguqulwa kwe-TTR Val122Ile okuvame ukutholakala kubantu bokhokho base-Afrika kungase kubhekwe njengento engasebenza ngokomtholampilo futhi kusheshe ukufinyelela ekwelashweni.
Ukwenziwa kusebenze kwe-guanylate cyclase/natriuretic peptide receptor A (GC-A/NPRA) ngamahomoni enhliziyo e-atrial kanye ne-brain natriuretic peptides (ANP kanye ne-BNP) kukhiqiza isithunywa sesibili i-cGMP.cGMP yenza kusebenze ukusayinda komfula kanye nemithelela yebhayoloji ye-ANP/NPRA ye-diuretic. , i-diuretic, i-vasodilatory, impendulo ye-antimitotic kanye nemiphumela ye-antihypertrophic yenhliziyo.Inkulumo yofuzo lwe-Npr1 (i-encoding GC-A/NPRA) ilawulwa yizisusa ezimbalwa zangaphandle nezangaphakathi, kodwa izindlela zamahomoni ne-epigenetic ezilamula ukulawulwa kwe-Npr1 akwaziwa.Inhloso yalolu cwaningo kwakuwukuhlola indima kavithamini D (vitD) ekulawuleni ukulotshwa kofuzo lwe-Npr1 kanye nenkulumo ngokulawula izici ze-epigenetic.
Ucwaningo lwethu lwe-bioinformatic lomgqugquzeli we-murine Npr1 luveze ubukhona bezinto ezine ze-vitD zokuphendula (ama-VDRE) endaweni -583 ukuya -495 endaweni yesayithi lokuqala lokuloba, ngokulandelana okuphelele kwe-VDRE okufana nokuvumelana okufana ne-VDRE. , izakhiwo zadluliselwa okwesikhashana kumaseli emisipha abushelelezi egundane le-thoracic aortic (RTASMC) kanye namaseli e-mouse mesangial (MMCs) futhi akalwa ngamakhithi okuhlola amabili e-luciferase.Umsebenzi wokuloba.
Ukuhlolwa kwe-Luciferase kubonise ukuthi ukwelashwa nge-vitamin D3 (1α,25-dihydroxy; VD3) kwandise umsebenzi womgqugquzeli we-Npr1 ngaphezu kwe-6-fold ngendlela encike kumthamo.Ukuhlaziywa kwe-Western blot kanye ne-densitometric kubonise ukuthi amazinga we-NPRA amaprotheni kuma-MMC anda kakhulu ngokukhula kwe-VD3 ukugxila, ukuphindaphinda okungu-3.5 kuma-RTASMC kanye nokuphindaphindeka okungu-4.7 kuma-RTASMC, futhi umphumela omkhulu wabonwa ku-100 nM.VD3 unyusa izinga leprotheyini le-vitD receptor (VDR) ngendlela encike kumthamo.Ebukhoneni be-VD3, i-histone Umsebenzi we-deacetylase (i-HDAC) wawuvinjelwe ngo-50% njengoba kulinganiswa umsebenzi we-HDAC/inhibition ELISA kit. Ngaphezu kwalokho, ukwelashwa nge-VD3 kuncishiswe ama-enzyme e-HDAC ekilasi I, i-HDAC1 kanye namazinga amaprotheni we-HDAC3, kanye nama-histone athuthukisiwe ancike kumthamo, i-H3 ezinsalela ze-lysine 9 kanye 14 (H3-K9/14 ac) kanye ne-lysine H4 endaweni ye-asidi engu-12 (H4-K14ac).
Imiphumela iphakamisa ukuthi i-VD3 ilawula nge-epigenetically i-Npr1 gene expression ngokulawula ukuguqulwa kwe-histone.Ukuhlonzwa kwethagethi ye-epigenetic yokusayina kwe-vitamin D njengabalawuli bokubhalwa kofuzo lwe-Npr1 kanye nokuvezwa kwamaprotheni kuzoba nemithelela ebalulekile yomfutho wegazi ophezulu kanye nokulawulwa kwenhliziyo nemithambo yegazi.
wabonisa ukuthi ukuboshwa kanye ne-superconductivity kuthuthukisa ukuqhutshwa kwe-intracellular ngamabili e-cardiomyocyte ehlukanisiwe, ukuthuthukisa ukuhlanganisa nokusebenza kwe-ventricular kwesokunxele.
Ukuhlolwa kwenziwa kusetshenziswa ubuhlakani bokwenziwa ngaphakathi kwamangqamuzana kusetshenziswa imiqondo ye-quantum ye-entanglement kanye ne-superconductivity;ukuqhutshwa kukagesi kwe-intracellular yonkana igebe elihlangene (GI) elidalwe yi-enalapril (E.) ne-angiotensin II (Ang II) kukalwa.E.Jova ku-1 ug / ml (25 ug / ml) ngaphezu kwemizuzu engu-4. I-plateau ifinyelelwa ku-valve ekugelezeni kwe-106% kusuka esikhwameni. lalingekho ithafa.
Sicabanga ukuthi i-plateau ifinyelelwa ngemva kokunciphisa ukuboshwa, kodwa hhayi nge-Ang II.Ezimweni ze-superconducting, i-E. coli yayiphumelela kakhulu ekuthuthukiseni ukuhlanganisa ama-myocyte ahlulekayo, ukuthuthukisa umsebenzi we-ventricular kwesokunxele.
Isifo seCoronavirus (COVID-19) sisukela ekuthelelekeni okungabonakali kuye ekuguleni okubi kakhulu okunokwehluleka kwezitho eziningi. Ucwaningo lwakamuva lubonise ukuhlobana phakathi kwamazinga aphansi e-serum lipid, okuyi-high-density lipoprotein (HDL), low-density lipoprotein (LDL), kanye nengqikithi i-cholesterol (TC), kanye nokuqina kwesifo se-COVID-19. Kodwa-ke, imiphumela iyashoda, futhi izinga lokuhlangana alaziwa okwamanje.
Senze ukubuyekezwa okuhlelekile kanye nokuhlaziywa kwe-meta-meta koku-1) umehluko kumazinga e-HDL, LDL, TC, kanye ne-triglyceride (TG) phakathi kweziguli ze-COVID-19 nezilawuli ezinempilo 2) ngokugula okukhulu nangaphandle kwe-COVID-19 Patient 3) COVID- Isiguli esingu-19 sashona futhi sasinda. Sifake ama-athikili asuka ku-PubMed and Embase kusukela ngomhlaka-1 Septhemba 2021. Sihlaziye umehluko wesilinganiso ohlanganisiwe (pMD) kumazinga e-lipid (mg/dL) wamaqembu angenhla sisebenzisa ukuhlaziya kwe-random-effects meta-analysis. futhi kuhlolwe ukuchema kokushicilela kusetshenziswa isakhiwo sefaneli.
Kuma-athikili abuyisiwe angu-441, ama-athikili angu-29 (ama-retrospective cohorts angu-26 kanye nama-3 azoba khona) ahlangabezane nenqubo yokufakwa, enengqikithi yabahlanganyeli abangu-256,721. Iziguli ezine-COVID-19 zazinamazinga aphansi e-HDL (pMD = -6.95) kanye ne-TC (pMD = -14.9) (Ithebula 1 kanye nomfanekiso 1).Amazinga e-LDL ne-TG awazange ahluke phakathi kweziguli ezine-COVID-19 nezingenayo.Iziguli ze-COVID-19 ezinzima zazinamazinga aphansi e-HDL (pMD = -4.4), LDL (pMD = -4.4 ) ne-TC (pMD = -10.4) uma kuqhathaniswa neziguli ze-COVID-19 ezingaqinile.Iziguli ezashona zazinamazinga aphansi e-HDL (pMD = -2.5), LDL (pMD = -10.6) ne-TC (pMD = -14.9). Amazinga e-TG awazange ahluke ebukhulwini noma ekufeni kwe-COVID-19. Akukho ukuhlaziya okungenhla okubonise ukuchema okuphawulekayo kwezibalo.
Ukuhlaziya kwethu kubonise ukuthi iziguli ezine-COVID-19 zazinamazinga aphansi e-lipid egazi uma kuqhathaniswa nezilawuli ezinempilo. Ezigulini ze-COVID-19, amazinga aphansi e-HDL, LDL, kanye ne-TC ayehlotshaniswa nokuqina nokufa. ukuvuvukala nokungasebenzi kahle kwesibindi.Amazinga e-lipid egazi angahlolwa njengezici ezingaba khona zokubikezela ezigulini ze-COVID-19.
I-Atrial kanye ne-brain natriuretic peptides (ANP kanye ne-BNP) ama-hormone ajikelezayo emvelaphi yenhliziyo adlala indima ebalulekile ekulawuleni umfutho wegazi kanye ne-homeostasis yoketshezi kanye nokwenza ngcono ukulungiswa kabusha kwenhliziyo ngemiphumela ye-vasodilatory ne-diuretic.Zombili i-ANP ne-BNP zisebenza ngokubophezela ku-transmembrane guanylate cyclase/natriuretic i-peptide receptor-A (GC-A/NPR-A).Ukuphazamiseka kwesistimu yofuzo lwe-Npr1 (umbhalo wekhodi we-GC-A/NPRA) kubangela ukugcwala kwevolumu, umfutho wegazi ophakeme, kanye nokwehluleka kwenhliziyo ehlangene.Nokho, indlela eyisisekelo ayizange ikhonjwe ngokunembile. .Inhloso yalolu cwaningo bekuwukuphenya ukuthi ingabe i-Npr1 idlala indima ebalulekile yini ekulawuleni i-glucose homeostasis kumagundane aphazamiseke ufuzo we-Npr1.
Abesilisa nabesifazane abadala (amaviki angu-16-18) i-Npr1 knockout haplotype (Npr1+/-, 1-copy), uhlobo lwasendle (Npr1+/+, 2-copy) kanye nokuphindaphindeka kofuzo (Npr1+ +/++, 4 -copy) Amagundane zazila ukudla amahora angu-16 futhi zakwazi ukufinyelela mahhala emanzini.Ukuphathwa ngomlomo kanye ne-intraperitoneal ye-glucose (2 g/kg isisindo somzimba) kwenziwa kumagundane ukuze kunqunywe ukuhlolwa kokubekezelela i-glucose ngomlomo (OGTT) kanye nokuhlolwa kwe-intraperitoneal glucose tolerance test (IPGTT). amazinga anqunywa ukopha komsila kumaminithi angu-0, 15, 30, 60, 90, kanye ne-120 kusetshenziswa i-AlphaTRAK Blood Glucose Monitoring System (Zoetis Inc, Kalamazoo, MI). indlela ye-tail-cuff (Visitech 2000).
Imiphumela ibonise ukuthi amazinga kashukela egazini kumagundane angamakhophi angu-2 (OGTT: 101 ± 4 mg/dL) enyuke afinyelela ezingeni eliphezulu emizuzwini eyi-15 ngemva kokuphathwa kwe-glucose (2 g/kg isisindo somzimba) futhi ehla afika eduze namazinga ayisisekelo emizuzwini eyi-120 kwabesilisa. .nabesifazane 98 ± 3 mg/dL, IPGT: abesilisa 100 ± 3 mg/dL, abesifazane 97 ± 4 mg/dL), kanti kumagundane ayikhophi engu-1, amazinga kashukela wegazi ahlala ephakeme ngisho nangemva kwemizuzu eyi-120 (OGTT: abesilisa 244 ± 6 mg/dL, female 220 ± 4 mg/dL, IPGT: owesilisa 250 ± 5 mg/dL, female 225 ± 6 mg/dL) uma kuqhathaniswa namagundane angu-2-copy.4-copy amagundane nawo abe namazinga eglucose aphansi kakhulu Amaminithi angu-120 (OGTT: 78 ± 3 mg/dL kwabesilisa, 73 ± 2 mg/dL kwabesifazane, IPGT: 76 ± 4 mg/dL kwabesilisa kanye 70 ± 3 mg/dL kwabesifazane).dL) uma kuqhathaniswa namagundane angamakhophi angu-2. I-SBP yayiphakeme kakhulu kumagundane angu-1 (134 ± 3 mmHg kwabesilisa kanye ne-125 ± 3 mmHg kwabesifazane) kunamagundane angu-2 (101 ± 2 mmHg kwabesilisa kanye ne-92 ± 2 mmHg kwabesifazane) .Ngokunjalo, amagundane angama-4-copy nawo abe ne-SBP ephansi kakhulu kunamagundane angama-2 (85 ± 3 mmHg kwabesilisa kanye ne-78 ± 2 mmHg kwabesifazane). Izinga eliphezulu le-glucose yegazi laliphansi kakhulu nge-OGTT uma kuqhathaniswa. nge-IPGTT.
Okutholakele kwamanje kukhombisa ukuthi i-Npr1 ivimbele kakhulu ukwenyuka okubukhali kwamazinga kashukela wegazi kulandela inselelo ye-glucose kanye nokunciphisa ukungabekezelelani kwe-glucose kumagundane ohlobo lwasendle kanye nezakhi zofuzo, okuphakamisa ukuthi i-Npr1 idlala indima ebalulekile ekulawuleni amazinga e-glucose kanye nokulahlekelwa kwe-Npr1 Action kuba nomthelela omubi. ukusebenza kwezinso nenhliziyo kumagundane aguquguqukayo.Lo msebenzi usekelwe yisibonelelo se-NIH (HL062147).
I-Central Arkansas Veterans Healthcare System John L. McClellan Memorial Veterans Hospital, Little Rock, Arkansas
Iziguli ezinesifo sezinso esingamahlalakhona (CKD) kanye ne-non-ST-segment elevation myocardial infarction (NSTEMI) zimelela inselele ebalulekile yomtholampilo.Isivumelwano phakathi kwezifundo ezingahleliwe kanye nokuhlola asiqiniseki.(1) Yenza izifundo ezingahleliwe kanye nezifundo zokubheka zisekela ukusetshenziswa kwe-invasive. Ukwelashwa ngezinga elifanayo (2) Ingabe imiphumela ithonywa amazinga okusebenza kwezinso?(3) Ingabe izinga lokufa liyafana nokwelashwa kwezidakamizwa kuphela ocwaningweni olungahleliwe nolokuhlola?
Ucwaningo lwakhethwa ngokusekelwe kulezi zindlela ezilandelayo: (1) imibiko engahleliwe noma yokuqaphela yeziguli ezine-NSTEMI kanye ne-CKD (2) inombolo yeziguli kanye nokufa okutholakalayo ukuze kutholakale ukwelashwa okuhlaselayo nokulondolozayo ezingeni ngalinye lomsebenzi wezinso, okuhlanganisa isilinganiso esilinganiselwe sokuhlunga kwe-glomerular (eGFR ) 30–60 kanye <30.Ukuhlaziywa kwemeta ngokuqhathaniswa kweqembu elincane kwaqedwa ngokubala izilinganiso zezinkinga zokufa okuvela ekwelapheni okuhlaselayo uma kuqhathaniswa nokugcinwa kwemithetho.
(1) Izifundo ezinhlanu ezingahleliwe kanye nezifundo ezine zokuhlola zahlangabezana nenqubo yokukhetha, enenani eliphelele leziguli ezingama-362,486 ezithola ukwelashwa okuhlaselayo noma okuvamile phakathi kuka-1994 no-2020.
(2) Ezifundweni ezingahleliwe, isilinganiso sezinkinga zokufa ngenxa yokwelashwa okuhlaselayo ezigulini ezine-eGFR 30-60 kwaba ngu-0.739, isikhathi sokuzethemba (CI) sasingu-0.382-1.431, p = 0.370.Ocwaningweni lokubheka lwe-eGFR 30-60, isilinganiso sezinkinga zokwelashwa okuhlaselayo kokufa sasingu-0.144, CI 0.012-0.892, p=0.037.
(3) Ezifundweni ezingahleliwe, isilinganiso sezinkinga zokufa ngenxa yokwelashwa okuhlaselayo ezigulini ezine-eGFR <30 kwaba ngu-0.790, CI 0.135–4.63, p=0.794.Ezifundweni zokubheka, iziguli ezine-eGFR <30 zinesilinganiso sokungafani esingu-0.384 se ukufa, CI 0.281–0.552, p<.05.
(4) Isilinganiso sengozi yokufa ezigulini ezine-eGFR 30-60 ezilashwa ngokwelashwa okulondolozayo kuphela kwakuyi-0.128 (CI -0.001-0.227) eqenjini lokucwaninga okungahleliwe kanye ne-0.44 (CI 0.227-0.6525) eqenjini locwaningo lokubuka, p< 0.01 .Ocwaningweni olungahleliwe Ingozi yeMedian yokufa yayiyi-0.345 (CI -0.103-0.794) ezigulini ezine-eGFR <30 ezithola ukwelashwa okulondolozayo kuphela kanye ne-0.463 (CI 0.00-0.926) ezifundweni zokubheka, p=0.579.
(1) Naphezu komphumela omuhle wokwelashwa okuhlaselayo kuzo zombili izifundo ezingahleliwe nezingenelele, isilinganiso sezinkinga zokufa ezifundweni zokubheka sasibaluleke ngokwezibalo.
(2) Ucwaningo lokuhlola luye lwabonisa ukuthi ukwelashwa okuhlaselayo kunesilinganiso esiphansi kakhulu sezinkinga zokufa ezigulini ezine-eGFR 30-60 kanye ne-eGFR <30.
(3) Iziguli eqenjini lokubuka zazinengozi enkulu yokufa ngokwelashwa okulondolozayo kuphela.
(4) Ucwaningo olwengeziwe luyadingeka ukuze kuthuthukiswe imodeli yokukhetha iziguli ezizozuza kakhulu ekwelashweni okuhlaselayo noma okuvamile.
(5) Imikhawulo yalolu cwaningo ihlanganisa umehluko wenani leziguli emaqenjini ocwaningo, ukuntuleka kwedatha ye-hemodynamic ne-angiographic ngokusho kwe-eGFR, kanye nokuthi kungenzeka ukuthi ezinye izifundo zihlanganisa iziguli ezine-angina pectoris engazinzile ngaphandle kwe-NSTEMI.
Naphezu kwentuthuko yezobuchwepheshe ku-cardiology, ukushaqeka kwe-cardiogenic njengenkinga ye-acute myocardial infarction kuseyinselelo yezokwelapha.Muva nje, i-National Cardiogenic Shock Management Standardization Campaign yethulwa e-United States, kanti i-National Cardiogenic Shock Initiative ihlose ukuthuthukisa ukusinda, ikakhulukazi ezigulini. nge-acute coronary syndrome (ACS) .Umgomo wethu kwakuwukuthola ukuthi ukushaqeka kwe-cardiogenic kwesibili kwe-ACS okudinga ukusekelwa kwemishini yokujikeleza kulawulwa kanjani esikhungweni sethu kanye nokuqhathanisa izici zomtholampilo phakathi kwabasindile nabangewona abasindile.
Ucwaningo olubuyela emuva lweziguli ezineminyaka engu-18-89 oludinga ukusekelwa kwesikhashana kokujikeleza kwegazi esimeni se-ACS e-University of Texas Lubbock Medical Center kusukela ngo-August 2018 kuya ku-August 2019. Kwaqhathaniswa abasindile nabangasindanga. ukuhlolwa kwesamba kwasetshenziselwa okuguquguqukayo kwezigaba nokuqhubekayo.
Kufakwe iziguli ezingama-39, ama-90% kwakungamadoda, iminyaka yobudala eyi-62, ama-62% anesifo sikashukela, kanti inkomba yesisindo somzimba yayiyi-29.01±5.84 kg/m2.Iphampu yebhaluni ye-Intra-aortic yayisetshenziswa kakhulu idivayisi yokusekela, elandelwa i-Impella (92% vs 8%).Izinga lokufa lilonke lalingu-18%.Izinga lokushaya kwenhliziyo eliphakanyisiwe kanye ne-lactate yokwamukelwa ngesikhathi sokusetshenziswa kokusekelwa kwemishini kwakuhlotshaniswa nokufa (105 bpm vs 83.91 bpm, p=0.02) (6.85 mmol/l vs 2.55 mmol/lp, 0.003. Percutaneous coronary intervention (PCI) Ukuba khona kokusekelwa kwangaphambili komshini noma i-coronary artery bypass grafting (CABG) ku-44% yeziguli kuhlotshaniswa nokusinda (53% vs 0% p=0.01) .
Izinga lenhliziyo eliphakanyisiwe kanye namazinga e-lactate ngesikhathi sokubekwa kokusekelwa kwemishini kuhlotshaniswa nokufa kweziguli ezine-cardiogenic shock secondary to acute coronary syndrome.Ukuqaliswa kokusekelwa kwemishini ngaphambi kokuba i-PCI ihlotshaniswe nokusinda.Kudingeka izifundo ezinkulu neziqinile ukuze kucaciswe lezi zinhlangano.
Ukuphatha i-hidradenitis suppurativa (HS) kungaba inselele.Ezimweni eziningi, izimpawu zeziguli ziba ngcono ngemva kokungenelela kokuqala kokulondoloza.Ngeshwa, ezinye izimo ziba ziphikisana futhi ziholela ekubuyiseleni kwezimonyo nokubuhlungu.Ukuhlinzwa kuvame ukusetshenziselwa ukumosha noma ukususa izicubu ezithintekile ukuze kuthuthukiswe ukuphulukiswa. .Sichaza isiguli esasingathandi ukuhlinzwa esathola ukwelashwa ngemisebe ye-electron beam.
Indoda eneminyaka engu-44 ubudala yethulwe ukujiya okusabalele kwezinqe, i-gluteal cleft, i-perineum, nethanga lamazwe amabili HS. Isiguli sasingathandi ukuchithwa ngokuhlinzwa nokwelashwa ngama-antibiotics kanye ne-corticosteroids. Sithole ukwelashwa kwe-electron beam radiation therapy nge-split course. Umthamo ophelele we-30 Gy kumithamo ehlukanisiwe eyi-10 futhi wagcina ukusabela okuyingxenye amasonto ama-2 ngemuva kokuqala kokwelashwa. Ukuhlolwa okuhlosiwe ngokomzimba phakathi nenyanga engu-1 yokwelashwa kubonise ukuncipha kwama-25% endaweni ephelele yokuvuvukala nokumakwa kokucaba kokuphakanyiswa. izindawo.Ngaleso sikhathi, iziguli zabika ukunciphisa okuzimele ebuhlungu kanye nokugeleza kwamanzi.Impendulo yayibhekwa njengeqinile ku-6 nezinyanga ze-12 ngemva kokwelashwa.
Ukwelashwa ngemisebe kunezinzuzo ezingavamile zezifo ezihlukahlukene eziyingozi futhi kuye kwafundwa ngemithamo ephansi (kwesinye isikhathi imithamo eyodwa) ekuphathweni kwe-HS. ukunciphisa imiphumela emibi.
Indawo yokwelapha yesiguli ebonisa i-hidradenitis suppurativa ezinqeni, i-gluteal cleft, i-perineum kanye namathanga amabili ngaphambi kokwelashwa.
Ukwelashwa ngemisebe ye-electron ephezulu kusebenza ngempumelelo ekwelapheni isifo esiyingozi futhi kunesithembiso se-HS.Isifundo sesamba semithamo nokuhlukaniswa kwezigaba kuyadingeka ukuze kuthuthukiswe futhi kuqondiswe ukusetshenziswa kwesikhathi esizayo.
Emphakathini jikelele wase-US, i-1 kubantu abangu-5,000 bane-myopathy ye-mitochondrial.Ukubonakaliswa komtholampilo kungahlukaniswa cishe ngezigaba ezintathu: i-ophthalmoplegia yangaphandle eqhubekayo, i-skeletal-CNS syndrome noma i-myopathy elula.Ukungajwayelekile kwenhliziyo kwenzeka ku-30-32% yamacala, ikakhulukazi njengoba i-hypertrophic cardiomyopathy, dilated cardiomyopathy, noma conduction abnormalities.Sethula icala lokuba buthakathaka komkhawulo ophansi, ubuhlungu, nokuvuvukala ngokuxilongwa kwe-muscle biopsy ye-mitochondrial myopathy.Incazelo yecala: Umfundi wesilisa oneminyaka engu-21 ubudala othweswe iziqu uthunyelwe esibhedlela sethu. ngemva kwamaviki angu-3 obuthakathaka bomlenze, ubuhlungu, nokuvuvukala ngemva kokufika e-United States evela eNdiya.Ukuhlolwa kwembula i-tachycardia, amaphuzu angu-2 + we-edema yomgodi emadolweni womabili, ubuthakathaka be-4/5 MRC-grade, ububele obumnene emaqenjini emisipha esondelene ne-distal yemikhawulo engenhla nephansi, akukho i-tendon reflexes ejulile, ukwehla kwezinyawo, kanye ne-ptosis yamazwe amabili kanye nokunyakaza okulinganiselwe kwe-extraocular.Imiphumela yaselabhorethri yokuqala yabonisa ukuthi i-creatinine kinase ikhuphuke ngo-691 IU / L, i-peptide ye-natriuretic yobuchopho inyuke ngo-3437 pg / mL, i-troponin inyuke ngo-47.1 ng/L, i-myoglobin inyuke ngo-195 ng/mL, futhi i-lactate inyuke ngo-7.7 mmol/L, i-serum bicarbonate yehle ngo-12 mmol/L. ukuchezuka ngokuvimba kwenqwaba yangaphambili kwesokunxele.I-X-ray yesifuba kanye ne-CT angiography yesifuba/isisu/i-pelvis ibonise ukukhuliswa kwenhliziyo kanye nomthamo omningi.Umbhede wakhe i-ECHO ibonise i-systemic hypokinesia ethambile, i-40-44% ephansi yokukhipha ingxenye, kanye nomfutho wegazi ophezulu wamaphaphu. isiguli sangeniswa egunjini labagula kakhulu ngenxa yokwehla kwengcindezi enkulu yokuphefumula.I-Ophthalmology yaqinisekisa i-ophthalmoplegia, ngaphandle kwe-cranial nerve palsy, i-myasthenia gravis, ne-retinitis pigmentosa.I-Gq1b antibody negative.Ukusebenza okubanzi kwe-autoimmune kanye nokutheleleka okuthelelanayo akunagalelo. we-rectus femoris muscle wesiguli wabonisa ama-fibers ahlakazekile aluhlaza okwesibhakabhaka kanye ne-cytochrome-c oxidase-negative enezicubu ezixhumene ze-perimuscular kanye ne-endomysial, ezihambisana ne-mitochondrial myopathy esebenzayo futhi engapheli.I-Endomyocardial biopsy ibonise i-lymphocytic myocarditis esebenzayo. I-metoprolol kanye ne-methylprednisolone.
I-Myopathy kufanele icatshangelwe ekuxilongweni okuhlukile kweziguli ezine-Guillain-Barre syndrome okusolakala ukuthi iyisifo.Sibika udaba oluthakazelisayo lwe-myopathy olunokubonakaliswa okuvelele kwenhliziyo.I-myositis ebonakala njenge-myocarditis kufanele iphakamise ukusola kwesifo se-mitochondrial.Okuhlangenwe nakho kwethu kugcizelela ukubaluleka kokusebenzisa ithimba le-interdisciplinary team. indlela yokuxilonga ama-pathologies angavamile ngokubandakanyeka okuguquguqukayo kwe-multisystem.
Inhloso yalolu cwaningo kwakuwukuhlola ukuthi kungenzeka yini ukuxilonga i-Gaisbock ezigulini ezine-polycythemia engapheli kanye nomfutho wegazi ophezulu.
Indoda eneminyaka engu-40 ubudala yaseCaucasus ekhuluphele yangeniswa esibhedlela inomlenze ovuvukalayo futhi yanda isidingo somoya-mpilo ngemuva kwamasonto amabili ilaliswe esibhedlela i-COVID-19 pneumonia. Ngemva kokubukeza umlando wezokwelapha wesiguli, yatholakala ine-hypertension engalashwa kanye ne-polycythemia. ishumi leminyaka ekuvakasheni okuningana.Umlando wezokwelapha wakamuva uhlanganisa ukuxilongwa kwe-deep vein thrombosis (DVT) emlenzeni ofanayo ezinyangeni ezimbili nesigamu ezedlule, kanye nokwelashwa nge-Xarelto.
Isiguli sabika umlando weminyaka engu-12 we-testosterone ephansi.Nokho, akazange asebenzise noma yiziphi izithako ze-testosterone ezinyangeni eziyisishiyagalolunye ezedlule.Wabika ukukhathala emini, ukuvuka njalo ebusuku, nokuhona njalo.Lesi siguli sasingakaze sibe nesifundo sokulala noma wasebenzisa i-CPAP.Isiguli sabhema ingxenye yethini likagwayi ohlafunwayo ngosuku iminyaka engu-13 elandelanayo, iphakethe elilodwa ngosuku, iminyaka engu-10 elandelanayo, futhi sayeka ukubhema eminyakeni engu-12 edlule.Wachitha ingxenye enkulu yokuphila kwakhe enza umsebenzi onzima embonini yokwakha.
Isikhathi sokuthumela: Jun-29-2022