Binciken Gyaran Ƙashin Ƙashin Ƙashin Ƙashin Ƙashin Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwar Ƙaƙwalwa

Atherosclerosis shine babban dalilin cututtukan cututtukan zuciya, wanda ya kasance jagorar duniya a cikin mace-mace.An nuna nau'in haɓakar insulin-kamar I (IGF1) don rage abubuwan da ke faruwa a cikin zuciya. /-) berayen sun ciyar da abinci mai kitse.Our baya in vitro sakamakon ya nuna cewa macrophages taka muhimmiyar rawa a mediating sakamakon IGF1 a atherosclerotic plaques, amma ainihin inji zauna m.We hypothesized cewa tsananin kara IGF1 matakan a macrophages zai. hana atherosclerosis.
Bayan kiwo novel macrophage-specific IGF1-overexpressing transgenic mice a cikin Apoe-/- baya (MF-IGF1 mice), mun tantance atherosclerotic plaque nauyi, kwanciyar hankali, da monocyte daukar ma'aikata.We accelerated ci gaban atherosclerosis ta ciyar da dabbobi a high- Abincin mai na tsawon watanni uku. Mun kuma tantance zubar da jini na cholesterol da samuwar kwayar kumfa a cikin vivo da in vitro.
Macrophage IGF1 overexpression downregulated plaque nauyi da 30%, rage plaque macrophages da 47%, da kuma inganta fasali da cewa stabilize da plaque phenotype. Monocyte daukar ma'aikata da aka rage da 70% a cikin MF-IGF1 mice da kuma daidaita tare da 27% raguwa a circulating matakan CXC. chemokine ligand 12 (CXCL12) .CXCL12 matakan sunadaran sunadaran an rage su a cikin plaques da peritoneal macrophages a cikin MF-IGF1 mice.In vitro, IGF1 gaba daya ya toshe oxidized low-density lipoprotein (oxLDL) - karuwa a CXCL12 mRNA transcription (98%) <0.01), kuma jiyya na IGF1 ya rage furotin CXCL12 (raguwar 56%, P <0.001).
CXCL12 yana rage maganganun ATP-binding cassette transporter A1 (ABCA1), mai mahimmancin jigilar cholesterol wanda ke daidaita ƙwayar cholesterol daga macrophages.Mun sami karuwa sau 2 a cikin matakan furotin ABCA1 a cikin macrophages na peritoneal da aka ware daga MF-IGF1 mice.Mun auna canje-canje. a cikin ƙwayar cholesterol ta hanyar ɗora macrophages peritoneal tare da oxLDL kuma sun sami karuwar 42% a cikin ƙwayar cuta a cikin mice MF-IGF1. Mun kuma sami karuwar 27% a cikin ƙwayar cholesterol a cikin kwayoyin THP-1 da aka bi da IGF1 (100 ng / mL) tare da apolipoprotein AI. kamar yadda mai karɓar cholesterol.
Sakamakonmu ya nuna cewa macrophage IGF1 yana rage atherosclerosis kuma yana rage CXCL12, wani chemokine da ke da hannu a cikin ci gaban atherosclerosis.IGF1 na iya rage CXCL12 ta hanyar rage yawan daukar ma'aikata na monocyte da karuwar ABCA1, ta haka yana yin tasiri na atheroprotective, ta haka ne ya kara yawan ƙwayar cholesterol.
Maye gurbi a cikin kwayar halittar TTR (rs76992529; Val122Ile) ana ganin su ne kawai a cikin daidaikun zuriyar Afirka (yawan yawan jama'a: 3-4%) wanda ke haifar da ɓarnawar rukunin transthyretin tetrameric, wanda ke samuwa a cikin transthyretin amyloidosis na gado.Degeneration (hATTR) yana tarawa a matsayin fibrils na amyloid na waje. Ƙididdiga tasirin wannan bambancin amyloidogenic TTR akan hadarin zuciya (HF) da dukan-sakamakon mace-mace a cikin babban, bambance-bambancen yanki na Afirka Amirkawa na iya ba da haske game da mahimmancin asibiti na wannan bambancin. .Mun kimanta mahalarta baƙar fata a cikin Nazarin Geographic da Kabilanci Daban-daban na Stroke (REGARDS) don nazarin haɗin gwiwar TTR Val122Ile maye gurbi tare da HF da duk-sakamakon mace-mace.
Mun ƙididdige masu halartar baƙar fata baƙar fata da aka ba da rahoton kai a cikin binciken REGARDS ba tare da HF ba a asali. An yi amfani da regression Poisson don kimanta abubuwan da ke faruwa na rashin ciwon zuciya da kuma mace-mace duka.Mun yi amfani da nau'i-nau'i-daidaitacce Cox regression model lissafin lissafin jama'a, asibiti da zamantakewa. dalilai, da kakannin kakannin halitta na Afirka don tantance haɗarin HF da duk sanadin mace-mace a cikin daidaikun mutane tare da bambancin jinsin TTR Val122Ile idan aka kwatanta da waɗanda ba tare da bambance-bambancen ba.
Daga cikin mahalarta baƙi 7,514 (tsakiyar shekaru: 64 shekaru; 61% mace), yawan yawan adadin TTR Val122Ile bambance-bambancen shine 3.1% (232 dillalai; 7,282 marasa ɗaukar hoto) . (95% CI: 11.5-21.9) tsakanin bambance-bambancen masu ɗaukar kaya da 7.2 (95% CI: 6.6-7.9) tsakanin bambance-bambancen masu ɗaukar nauyi. : 1.72-3.53]; P <0.0001) . Abubuwan da suka faru na duk abin da ke haifar da mace-mace (a kowace shekara 1000) shine 41.5 (95% CI: 34.6-49.7) tsakanin masu jigilar kayayyaki da 33.9 (95% CI: 52.7-3) tsakanin bambance-bambancen da ba masu ɗaukar kaya ba.Val122Ile bambance-bambancen masu ɗaukar nauyi suna da haɗari mafi girma na duk abin da ke haifar da mace-mace idan aka kwatanta da waɗanda ba masu ɗaukar kaya ba (HR: 1.44 [95% CI: 1.18-1.76]; P=0.0004) .TTR bambance-bambancen matsayi da jinsi bai yi ba. yin hulɗa tare da HF da duk sakamakon mace-mace.
A cikin babban rukuni na baƙar fata Amirkawa, mun nuna cewa maye gurbin amyloid Val122Ile a cikin kwayar halittar TTR yana da alaƙa da kusan 2.5-ninka mafi girma na HF da kuma kusan 40% mafi girma na haɗari na mutuwa. hanyoyin kwantar da hankali, kasancewar maye gurbi na TTR Val122 da aka saba samu a cikin mutanen kakannin Afirka ana iya ɗaukarsu a matsayin mai aiki a asibiti da kuma hanzarta samun magani.
Kunna guanylate cyclase / natriuretic peptide receptor A (GC-A / NPRA) ta hanyar cardiac hormones atrial da kwakwalwa natriuretic peptides (ANP da BNP) suna samar da manzo na biyu cGMP.cGMP yana kunna alamar ƙasa da tasirin nazarin halittu na ANP / NPRA don diuretic. , diuretic, vasodilatory, martani na antimitotic da cututtukan cututtukan zuciya na zuciya.Maganar Npr1 gene (encoding GC-A / NPRA) an tsara shi ta wasu abubuwan motsa jiki na waje da na ciki, amma tsarin hormonal da epigenetic wanda ke daidaita tsarin Npr1 ba a sani ba. na wannan binciken shine don bincika rawar bitamin D (vitD) a cikin daidaita rubutun Npr1 da magana ta hanyar daidaita abubuwan epigenetic.
Binciken mu na bioinformatic na murine Npr1 mai talla ya bayyana kasancewar abubuwan amsawar vitD guda huɗu (VDREs) a cikin yankin -583 zuwa -495 na wurin fara rubutun, tare da cikakken jerin ra'ayi kamar VDRE. , An canza abubuwan da aka gina a cikin ɗan gajeren lokaci a cikin al'adar bera thoracic aortic smooth muscle cells (RTASMCs) da linzamin kwamfuta mesangial Kwayoyin (MMCs) da kuma auna don dual luciferase kits assay.Ayyukan rubutu.
Luciferase assay ya nuna cewa jiyya tare da bitamin D3 (1α,25-dihydroxy; VD3) ya karu da aikin Npr1 mai gabatarwa fiye da 6-ninka a cikin hanyar da ta dace da kashi. maida hankali, 3.5-ninka a cikin RTASMCs da 4.7-ninki a cikin RTASMCs, kuma an lura da iyakar sakamako a 100 nM.VD3 yana ƙara yawan furotin na mai karɓa na vitD (VDR) a cikin hanyar da ta dace. A gaban VD3, histone. Ayyukan deacetylase (HDAC) an hana 50% kamar yadda aka auna ta hanyar aikin HDAC / hanawa ELISA kit. Bugu da ƙari kuma, jiyya tare da VD3 rage aji I HDAC enzymes, HDAC1 da HDAC3 matakan gina jiki, da kuma haɓakar haɓakar kwayoyin halitta, H3 a lysine residues 9 da 14 (H3-K9/14 ac) da lysine H4 a ragowar acid 12 (H4-K14ac).
Sakamakon ya nuna cewa VD3 epigenetically yana daidaita maganganun Npr1 ta hanyar sarrafa gyare-gyare na histone.Bayyana maƙasudin epigenetic na siginar bitamin D a matsayin masu kula da rubutun Npr1 da kuma bayanin furotin zai sami tasiri mai mahimmanci ga hauhawar jini da tsarin zuciya na zuciya.
ya nuna cewa haɗakarwa da haɓakawa sun inganta haɓakar intracellular a cikin nau'i-nau'i na keɓaɓɓen cardiomyocytes, inganta haɗin gwiwa da aikin ventricular na hagu.
An yi gwaje-gwajen ta amfani da hankali na wucin gadi a cikin sel ta amfani da ra'ayoyin ƙididdiga na haɗuwa da haɓakawa;Gudanar da wutar lantarki ta cikin cell a cikin tazarar junctional (GI) wanda enalapril (E.) da angiotensin II (Ang II) ya haifar an auna.E.An yi allurar a 1 ug / ml (25 ug / ml) a kan minti 4. An kai wani faranti a cikin bawul a 106% ya kwarara daga jakar.Ang II. An yi allurar a 1 ug / min, an rage GI (55%) kuma babu plateau.
Muna tsammanin an kai wani fili bayan an rage haɗakarwa, amma ba tare da Ang II ba. A cikin yanayin da ya fi dacewa, E. coli ya fi tasiri wajen inganta haɗin kai na kasawar myocytes, inganta aikin ventricular hagu.
Cutar Coronavirus (COVID-19) tana fitowa daga kamuwa da cutar asymptomatic zuwa rashin lafiya mai tsanani tare da gazawar gabbai da yawa.Bincike na baya-bayan nan ya nuna alaƙa tsakanin ƙananan matakan lipid na jini, wato high-density lipoprotein (HDL), low-density lipoprotein (LDL), da kuma duka. cholesterol (TC), da cutar COVID-19. Duk da haka, sakamakon ba shi da daidaito, kuma ba a san iyakar ƙungiyar a halin yanzu ba.
Mun yi bita na tsari da meta-bincike na 1) bambance-bambance a cikin matakan HDL, LDL, TC, da triglyceride (TG) tsakanin marasa lafiya na COVID-19 da kulawar lafiya. 19 majiyyaci ya mutu kuma ya tsira. Mun haɗa da labarai daga PubMed da Embase har zuwa Satumba 1, 2021. Mun yi nazarin bambancin ma'anar ma'ana (pMD) a cikin matakan lipid (mg/dL) na ƙungiyoyin da ke sama ta amfani da bazuwar tasirin meta-bincike. da kuma tantance son zuciya ta wallafe-wallafe ta amfani da makircin mazurari.
Daga cikin labaran 441 da aka dawo dasu, labarai 29 (26 na baya-bayan nan da 3 masu zuwa) sun cika ka'idojin haɗawa, tare da jimlar mahalarta 256,721. Marasa lafiya tare da COVID-19 suna da ƙananan matakan HDL (pMD = -6.95) da TC (pMD = -14.9) (Table 1 da Figure 1) .LDL da TG matakan ba su bambanta tsakanin marasa lafiya tare da kuma ba tare da COVID-19 ba.Masu fama da COVID-19 suna da ƙananan matakan HDL (pMD = -4.4), LDL (pMD = -4.4). ) da TC (pMD = -10.4) idan aka kwatanta da marasa lafiya na COVID-19. Marasa lafiya da suka mutu suna da ƙananan matakan HDL (pMD = -2.5), LDL (pMD = -10.6) da TC (pMD = -14.9). Matakan TG ba su bambanta da tsananin COVID-19 ko mace-mace ba. Babu ɗaya daga cikin binciken da ke sama da ya nuna nuna son kai a cikin ƙididdiga.
Bincikenmu ya nuna cewa marasa lafiya da ke da COVID-19 suna da ƙananan matakan lipid na jini idan aka kwatanta da kulawar lafiya. A cikin marasa lafiya na COVID-19, ƙananan matakan HDL, LDL, da TC suna da alaƙa da tsanani da mutuwa. kumburi da tabarbarewar hanta. Za a iya bincika matakan lipid na jini azaman abubuwan da za su iya tantancewa a cikin marasa lafiya na COVID-19.
Atrial da kuma kwakwalwa natriuretic peptides (ANP da BNP) suna zazzage hormones na asalin zuciya wanda ke taka muhimmiyar rawa wajen daidaita karfin jini da kuma homeostasis na ruwa da inganta gyaran zuciya ta hanyar vasodilatory da diuretic effects.Dukansu ANP da BNP suna aiki ta hanyar ɗaure zuwa transmembrane guanylate cyclase / natriuretic peptide receptor-A (GC-A/NPR-A) .Tsarin tsarin na Npr1 gene (encoding GC-A/NPRA) yana haifar da nauyin girma, hauhawar jini, da ciwon zuciya. .Manufar wannan binciken shine don bincika ko Npr1 tana taka muhimmiyar rawa wajen daidaita glucose homeostasis a cikin berayen Npr1 da suka rushe.
Manya maza da mata (16-18 makonni) Npr1 knockout haplotype (Npr1+/-, 1-copy), daji-type (Npr1+/+, 2-copy) da kuma kwayar halitta kwafi (Npr1+ +/++, 4 -copy) Mice an yi azumi na sa'o'i 16 kuma suna da damar samun ruwa kyauta. An gudanar da maganin glucose na baki da na intraperitoneal (2 g / kg nauyin jiki) a cikin mice don ƙayyade gwajin haƙuri na glucose na baka (OGTT) da gwajin haƙuri na glucose na ciki (IPGTT) . An ƙaddara matakan ta hanyar zubar da wutsiya a 0, 15, 30, 60, 90, da 120 minutes ta amfani da AlphaTRAK Blood Glucose Monitoring System (Zoetis Inc, Kalamazoo, MI). Hanyar wutsiya (Visitech 2000).
Sakamakon ya nuna cewa matakan glucose na jini a cikin mice guda biyu (OGTT: 101 ± 4 mg / dL) ya karu zuwa matsakaicin a cikin mintuna 15 bayan gudanarwar glucose (2 g / kg jiki) kuma ya ragu zuwa kusa da matakan basal a cikin mintuna 120 a cikin maza. .da mata 98 ​​± 3 mg / dL, IPGT: maza 100 ± 3 mg / dL, mata 97 ± 4 mg / dL), yayin da a cikin 1-kwafin mice, matakan glucose na jini ya kasance mai girma ko da bayan mintuna 120 (OGTT: maza 244 ± 6 mg/dL, mace 220 ± 4 mg/dL, IPGT: namiji 250 ± 5 mg/dL, mace 225 ± 6 mg/dL) idan aka kwatanta da 2-kwafin mice.4-kwafin beraye kuma sun sami raguwar matakan glucose na jini sosai a Minti 120 (OGTT: 78 ± 3 mg/dL ga maza, 73 ± 2 mg/dL ga mata, IPGT: 76 ± 4 mg/dL ga maza da 70 ± 3 mg/dL ga mata).dL) idan aka kwatanta da 2-copy mice. SBP ya kasance mafi girma a cikin 1-copy mice (134 ± 3 mmHg a cikin maza da 125 ± 3 mmHg a cikin mata) fiye da 2-copy mice (101 ± 2 mmHg a cikin maza da 92 ± 2 mmHg a cikin mata).Haka kuma, 4-copy mice kuma yana da ƙananan SBP fiye da 2-copy mice (85 ± 3 mmHg a cikin maza da 78 ± 2 mmHg a cikin mata).Mafi girman matakin glucose na jini ya ragu sosai tare da OGTT idan aka kwatanta. tare da IPGTT.
Binciken da aka yi a yanzu ya nuna cewa Npr1 ya hana haɓakar matakan glucose na jini bayan ƙalubalen glucose da haɓaka rashin haƙuri na glucose a cikin nau'in daji da nau'in berayen da aka kwafi, yana nuna cewa Npr1 yana taka muhimmiyar rawa wajen daidaita matakan glucose da asarar Npr1 Action yana da illa. aikin koda da zuciya a cikin mice mutant.Wannan aikin yana goyan bayan kyautar NIH (HL062147).
Tsarin Kiwon Lafiyar Tsohon Tsohon Tsohon Arkansas John L. McClellan Memorial Veterans Hospital, Little Rock, Arkansas
Marasa lafiya tare da cututtukan koda na yau da kullun (CKD) da marasa ST-segment elevation myocardial infarction (NSTEMI) suna wakiltar ƙalubalen ƙalubale na asibiti. Yarjejeniyar tsakanin bazuwar da binciken lura ba shi da tabbas. jiyya daidai gwargwado (2) Shin matakan aikin koda suna tasiri sakamakon sakamako?(3) Shin adadin mace-mace iri ɗaya ne tare da maganin ƙwayoyi kaɗai a cikin bazuwar da kuma na lura?
An zaɓi nazarin bisa ga ma'auni masu zuwa: (1) bazuwar ko rahotanni na lura da marasa lafiya tare da NSTEMI da CKD (2) adadin marasa lafiya da mace-mace da ke samuwa don cin zarafi da ra'ayin mazan jiya a kowane mataki na aikin koda, ciki har da ƙididdigar ƙididdigar glomerular (eGFR). ) 30-60 da <30.An kammala nazarin meta-bincike tare da kwatancen rukuni ta hanyar ƙididdige ƙididdige ƙididdiga na mace-mace daga cin zarafi tare da jiyya na mazan jiya.
(1) Nazarin bazuwar guda biyar da binciken lura guda huɗu sun cika ka'idojin zaɓi, tare da jimillar marasa lafiya 362,486 waɗanda ke karɓar cin zarafi ko ra'ayin mazan jiya tsakanin 1994 da 2020
(2) A cikin binciken da bazuwar, rabon rashin daidaituwa ga mutuwa saboda jiyya mai lalacewa a cikin marasa lafiya tare da eGFR 30-60 shine 0.739, tazarar amincewa (CI) shine 0.382-1.431, p = 0.370.A cikin binciken lura na eGFR 30-60, Matsakaicin rashin daidaituwa don maganin cutarwa ga mutuwa shine 0.144, CI 0.012-0.892, p=0.037.
(3) A cikin binciken da bazuwar, ƙimar rashin daidaituwa ga mutuwa saboda jiyya mai lalacewa a cikin marasa lafiya tare da eGFR <30 shine 0.790, CI 0.135-4.63, p = 0.794. mutuwa, CI 0.281-0.552, p<.05.
(4) Ma'anar haɗarin mutuwa a cikin marasa lafiya tare da eGFR 30-60 da aka bi da su tare da magani mai ra'ayin mazan jiya kawai shine 0.128 (CI-0.001-0.227) a cikin rukunin binciken da bazuwar da 0.44 (CI 0.227-0.6525) a cikin ƙungiyar nazarin lura, p< 0.01 .A cikin binciken bazuwar Matsakaicin haɗarin mutuwa shine 0.345 (CI-0.103-0.794) a cikin marasa lafiya tare da eGFR <30 suna karɓar magani mai ra'ayin mazan jiya kawai da 0.463 (CI 0.00-0.926) a cikin nazarin lura, p=0.579.
(1) Duk da kyakkyawan sakamako na jiyya na ɓarna a cikin binciken bazuwar da kuma shiga tsakani, rabon rashin daidaituwa ga mutuwa a cikin binciken lura yana da mahimmancin ƙididdiga.
(2) Nazarin lura ya nuna cewa maganin cutarwa yana da ƙarancin ƙarancin ƙima ga mutuwa a cikin marasa lafiya tare da eGFR 30-60 da eGFR <30.
(3) Marasa lafiya a cikin ƙungiyar lura suna da haɗari mafi girma na mutuwa tare da magani mai ra'ayin mazan jiya kawai.
(4) Ana buƙatar ƙarin bincike don samar da samfuri don zaɓar marasa lafiya waɗanda za su amfana da mafi yawan maganin cutarwa ko ra'ayin mazan jiya.
(5) Ƙayyadaddun wannan binciken sun haɗa da bambance-bambance a cikin adadin marasa lafiya a cikin ƙungiyoyin binciken, rashin bayanan hemodynamic da angiographic bisa ga eGFR, da yiwuwar cewa wasu nazarin sun haɗa da marasa lafiya tare da angina pectoris maras kyau banda NSTEMI.
Duk da ci gaban fasaha a cikin cardiology, Cardiogenic rawar jiki kamar rikitarwa kamun kamfen na mama da na iya gabatar da ƙalubalen likita, kuma musamman, a cikin marasa lafiya tare da ciwo mai tsanani na jijiyoyin jini (ACS) .Manufarmu shine don ƙayyade yadda cardiogenic shock na biyu zuwa ACS da ke buƙatar tallafin jini na inji a cikin ma'aikatarmu da kuma kwatanta halayen asibiti tsakanin masu tsira da wadanda ba su tsira ba.
Wani bincike na baya-bayan nan game da marasa lafiya masu shekaru 18-89 da ke buƙatar tallafin inji na wucin gadi a cikin saitin ACS a Cibiyar Kiwon Lafiya ta Jami'ar Texas Lubbock daga Agusta 2018 zuwa Agusta 2019. An kwatanta fitar da tsira da waɗanda ba su tsira ba.Ainihin gwajin Fisher da darajar Wilcoxon- An yi amfani da jimlar gwajin don nau'i-nau'i da masu ci gaba.
An haɗa jimlar marasa lafiya 39, 90% maza ne, matsakaicin shekarun shekaru 62, 62% suna da ciwon sukari, kuma ma'anar ma'aunin jiki shine 29.01± 5.84 kg/m2.Intra-aortic balloon pump shine mafi yawan amfani da injin balloon. na'urar tallafi, wanda Impella ya biyo baya (92% vs 8%). Yawan mace-mace gabaɗaya ya kasance 18%.Ƙaƙƙarfan ƙwayar zuciya da lactate akan shiga yayin amfani da tallafin injina yana da alaƙa da mace-mace (105 bpm vs 83.91 bpm, p=0.02) (6.85) mmol/l vs 2.55 mmol/lp, 0.003. Percutaneous intercutaneous intercutaneous intervention (PCI) Kasancewar goyon bayan injiniya na farko ko ƙwayar jijiyoyin jini (CABG) a cikin 44% na marasa lafiya an haɗa su da rayuwa (53% vs 0% p=0.01) .
Ƙwaƙwalwar ƙwayar zuciya da matakan lactate a lokacin sanyawa na goyon bayan injiniya suna hade da mace-mace a cikin marasa lafiya tare da cututtukan zuciya na cardiogenic zuwa m ciwon zuciya. Farawar goyon bayan injiniya kafin PCI ya haɗu da rayuwa. Ana buƙatar karatu mafi girma kuma mafi mahimmanci don bayyana waɗannan ƙungiyoyi.
Sarrafa hidradenitis suppurativa (HS) na iya zama ƙalubale.A lokuta da yawa, alamun marasa lafiya sun inganta bayan shiga tsakani na farko. .Mun bayyana majiyyaci wanda ya ƙi yin aikin tiyata wanda ya yi amfani da hasken wutar lantarki a saman.
Wani mutum mai shekaru 44 da haihuwa ya gabatar da wani nau'i mai ban sha'awa na gindi, gluteal cleft, perineum, da cinya biyu HS. Mai haƙuri ya kasance mai ƙyama ga lalatawar tiyata da magani tare da maganin rigakafi da corticosteroids. jimlar kashi na 30 Gy a cikin kashi 10 na kashi 10 kuma ya ci gaba da mayar da martani ga 2 makonni bayan fara magani. Maƙasudin nazarin jiki a cikin watan 1 na jiyya ya nuna raguwar 25% a cikin duka yanki na kumburi da alama flattening na tashe. yankuna.A wannan lokacin, marasa lafiya sun ba da rahoton raguwar ra'ayi na raɗaɗi a cikin ciwo da magudanar ruwa.An yi la'akari da amsawar a cikin watanni 6 da 12 bayan jiyya.
Maganin Radiation yana da fa'idodin anecdotal ga cututtuka iri-iri kuma an yi nazari a cikin ƙananan allurai (wani lokacin allurai guda ɗaya) a cikin kulawar HS. Mun zaɓi yin amfani da hanyar tsagawa wanda muka yi imani shine mafi aminci kuma mai yiwuwa mafi dawwama cikin sharuddan rage illa.
Yankin jiyya na marasa lafiya yana nuna hidradenitis suppurativa a cikin gindi, ƙwanƙwasa gluteal, perineum da cinyoyin biyu kafin magani.
Ƙwararren wutar lantarki na lantarki na radiation farfesa yana da tasiri wajen magance cututtuka mara kyau kuma yana da alƙawari don HS. Nazari na jimlar kashi da tsarin juzu'i ana buƙatar don ingantawa da jagorantar amfani da gaba.
A cikin yawan jama'ar Amurka, 1 a cikin 5,000 mutane suna da myopathy. hypertrophic cardiomyopathy, dilated cardiomyopathy, ko conduction abnormalities.Muna gabatar da wani hali na biyu ƙananan ƙananan ƙafafu, ciwo, da kumburi tare da ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar ƙwayar cuta. bayan makonni 3 na rauni na ƙafafu, zafi, da kumburi bayan isa Amurka daga Indiya. Binciken ya nuna tachycardia, 2+ maki na pitting edema a cikin gwiwoyi biyu, 4/5 MRC-grade rauni, m taushi a cikin kusanci da kuma m tsoka kungiyoyin. na babba da ƙananan ƙananan ƙafafu, babu zurfin ƙwayar tsoka mai zurfi, raguwar ƙafar ƙafa, da ptosis na biyu da kuma ƙuntataccen motsi na waje. Sakamakon binciken farko ya nuna creatinine kinase ya karu da 691 IU / L, peptide na natriuretic na kwakwalwa ya karu da 3437 pg / mL, troponin ya karu da 47.1 ng/L, myoglobin ya karu da 195 ng/mL, kuma lactate ya karu da 7.7 mmol /L, serum bicarbonate ya ragu da 12 mmol/L. Sakamakon huda na Lumbar da ake zargin Guillain-Barre ciwo ba shi da tabbas saboda taps mai rauni. Electrocardiogram ya nuna hagu axis. karkacewa tare da gungu na baya na hagu. X-ray na ƙirji da CT angiography na ƙirji / ciki / ƙashin ƙugu sun nuna haɓakar zuciya da yawa da yawa. A gefen gadon sa na ECHO ya nuna hypokinesia na tsarin hagu mai sauƙi, 40-44% ƙananan ejection juzu'i, da hauhawar hauhawar jini na huhu. An shigar da majiyyaci zuwa sashin kulawar gaggawa na likita saboda raguwar matsakaicin matsananciyar motsa jiki.Ophthalmology ya tabbatar da ophthalmoplegia, ban da kumburin jijiyoyi na cranial, myasthenia gravis, da retinitis pigmentosa.Gq1b antibody negative.Extensive autoimmune da kamuwa da cuta aiki ba da gudummawar muscle. na majinyacin duburar tsokar femoris mai haƙuri ya nuna tarwatsewar shuɗi da cytochrome-c oxidase-korau zaruruwa tare da ƙãra perimuscular da endomysial connective nama, daidai da aiki da kuma na kullum primary mitochondrial myopathy.Endomyocardial biopsy ya nuna aiki lymphocytic myocarditis.Mai haƙuri da aka samu nasarar bi da furosemide, Metoprolol, da kuma methylprednisolone.
Ya kamata a yi la'akari da myopathy a cikin bambancin ganewar cututtuka na marasa lafiya da ake zargi da ciwo na Guillain-Barre. Muna bayar da rahoton wani lamari mai ban sha'awa na myopathy tare da manyan bayyanar cututtuka na zuciya. hanya don gano cututtukan cututtukan da ba kasafai ba tare da shigar da tsarin tsarin da yawa.
Manufar wannan binciken shine don gano yiwuwar gano Gaisbock a cikin marasa lafiya da polycythemia na kullum da hauhawar jini.
An shigar da wani mutumin Caucasian mai shekaru 40 mai kiba a asibiti tare da kumburin ƙafafu da yawa kuma yana ƙaruwa da buƙatar iskar oxygen bayan makonni biyu na asibiti tare da ciwon huhu na COVID-19. shekaru goma a ziyara da yawa. Tarihin likita na kwanan nan ya haɗa da ganewar asali na thrombosis mai zurfi (DVT) a cikin kafa guda biyu da rabi da suka wuce, da magani tare da Xarelto.
Mai haƙuri ya ba da rahoton tarihin shekaru 12 na ƙananan testosterone. Duk da haka, bai yi amfani da wani maganin testosterone a cikin watanni tara da suka wuce ba. ya yi amfani da CPAP.Majinyacin ya sha taba rabin gwangwani na taba a kowace rana tsawon shekaru 13 a jere, fakiti daya a rana, tsawon shekaru 10 a jere, kuma ya daina shan taba shekaru 12 da suka wuce. Ya shafe yawancin rayuwarsa yana aiki tukuru a masana'antar gine-gine.

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  • Lokacin aikawa: Juni-29-2022