tbuckley/cabot-search huggingface dataset:
Clinical Records
Authors: H. Lee
Journal: BMJ (1864)

d'elite-who have joined neither party, rejecting the extreme ideas alike of the ultra worshippers of bleeding and of its enemiiies.There have always been, and always will be, patricians of this high class in medicine."Elsewhere he sums up, and still in golden words, the actual value of bleeding."It miiay be said that, as a rule, the partisans of bleeding over- estimate the value of its effects and the necessity for its use; and that, on the other hand, those who rarely resort to bleeding have ani unreasonable dread of its consequencees.It is not tiue that nuiiibers die froimi bleeding, as some would have us believe; and still less is it true that those who rarely ever bleed lose as miiany patients as the partisans of bleeding say they (lo.Daily observation in hospitals shows the fallacy of both these conclusionis; and the truth is, that it is not easy to distiniguislh between bleedings which are useful and necessary, and bleedings wlich are hurtful and injurious."LTo be continued.
Abstract 222: Role of Pathologic Calpain Activity in Post-Cardiac Arrest Hypothermic Targeted Temperature Management
Authors: Tulasi R Jinka, Adam Chalek, Jacob Katzman, Xiaodan Ren, Robert W Neumar
Journal: Circulation (2018)

Objective: Optimization of post-cardiac arrest hypothermic-targeted temperature management (HTTM) is limited by an inadequate understanding of the fundamental mechanisms of action. This study tested the hypothesis that post-cardiac arrest HTTM reduces delayed secondary neuronal cytosolic Ca 2+ overload that causes pathologic calpain activity and neuronal death after cardiac arrest (CA) Methods: Male Long Evens rats were subjected to 8-minute asphyxial CA (ACA) followed by CPR. Rats that achieved return of spontaneous circulation (ROSC) were block randomized to normothermic- targeted temperature management (NTTM; n=13), hypothermic-TTM at 36 o C (HTTM-36;n=13) or 33 o C (HTTM-33;n=10). HTTM was initiated 1h after ROSC and maintained for 24h. Neurologic function score was assessed daily. Rats were euthanized at 48h post-ROSC. Regional brain homogenates were generated in a subset of animals for Western blot analysis of calpain-cleaved alpha-spectrin as a measure of pathologic calpain activity (n=6/group). Sham rats were used as uninjured controls (n=9) Results: Survival at 48h post-ROSC was 69%, 69%, and 90% in the NTTM, HTTM-36 and HTTM-33 groups respectively (p&gt;0.05: chi-squared). Survival with good neurologic function (GNF: defined as NFS &gt; 450 out of 500) was 0%, 15%, and 60% in the NTTM, HTTM-36 and HTTM-33 groups respectively (p&lt;0.05 for HTTM-33 vs. HTTM-36 and NTTM: chi-squared). Compared to NTTM, pathologic calpain activity in the hippocampus, cortex, caudoputamen, and cerebellum was decreased by 23±20%, 38±56%, 40±55%, 62±20% in the HTTM-36 groups and 33±13%, 55±72%, 66±89%, 69±17% in the HTTM-33 group respectively (p &lt;0.05 for HTTM-33 and HTTM-36 cerebellum, p&gt; 0.05 for all other regions: ANOVA, Tukey’s post-hoc) Conclusion: In this rat model of asphyxial cardiac arrest, HTTM with a target temperature of 33°C improved 48-hour survival with GNF compared to HTTM with a target temperature of 36°C and NTTM. Post-cardiac arrest regional brain calpain activity was significantly reduced with HTTM at 33°C and 36°C compared to NTTM in the cerebellum, but not other brain regions. Further work is needed to explore the potential causal link between the reduction of pathologic calpain activity and the neuroprotective effect of post-cardiac arrest HTTM
Risk Factors and Prognosis of Early Posttraumatic Seizures in Moderate to Severe Traumatic Brain Injury
Authors: Joshua Laing, Belinda Gabbe, Zhibin Chen, Piero Perucca, Patrick Kwan, Terence J. O’Brien
Journal: JAMA Neurology (2022)

Early posttraumatic seizures (EPS) that may occur following a traumatic brain injury (TBI) are associated with poorer outcomes and development of posttraumatic epilepsy (PTE).To evaluate risk factors for EPS, associated morbidity and mortality, and contribution to PTE.Data were collected from an Australian registry-based cohort study of adults (age ≥18 years) with moderate to severe TBI from January 2005 to December 2019, with 2-year follow-up. The statewide trauma registry, conducted on an opt-out basis in Victoria (population 6.5 million), had 15 152 patients with moderate to severe TBI identified via Abbreviated Injury Scale (AIS) head severity score, with an opt-out rate less than 0.5% (opt-out n = 136).EPS were identified via International Statistical Classification of Diseases, Tenth Revision, Australian Modification (ICD-10-AM) codes recorded after the acute admission. Outcome measures also included in-hospital metrics, 2-year outcomes including PTE, and post-discharge mortality. Adaptive least absolute shrinkage and selection operator (LASSO) regression was used to build a prediction model for risk factors of EPS.Among the 15 152 participants (10 457 [69%] male; median [IQR] age, 60 [35-79] y), 416 (2.7%) were identified with EPS, including 27 (0.2%) with status epilepticus. Significant risk factors on multivariable analysis for developing EPS were younger age, higher Charlson Comorbidity Index, TBI sustained from a low fall, subdural hemorrhage, subarachnoid hemorrhage, higher Injury Severity Score, and greater head injury severity, measured using the AIS and Glasgow Coma Score. After adjustment for confounders, EPS were associated with increased ICU admission and ICU length of stay, ventilation and duration, hospital length of stay, and discharge to inpatient rehabilitation rather than home, but not in-hospital mortality. Outcomes in TBI admission survivors at 24 months, including mortality (relative risk [RR] = 2.14; 95% CI, 1.32-3.46; P = .002), development of PTE (RR = 2.91; 95% CI, 2.22-3.81; P < .001), and use of antiseizure medications (RR = 2.44; 95% CI, 1.98-3.02; P < .001), were poorer for cases with EPS after adjustment for confounders. The prediction model for EPS had an area under the receiver operating characteristic curve of 0.72 (95% CI, 0.66-0.79), sensitivity of 66%, and specificity of 73% in the validation set.We identified important risk factors for EPS following moderate to severe TBI. Early posttraumatic seizures were associated with longer ICU and hospital admissions, ICU ventilation, and poorer 24-month outcomes including mortality and development of PTE.
Address in Medicine
Authors: W. M. Ord
Journal: BMJ (1884)

cine succeed, there will be still only too ample scope for the physician and surgeon.It is for us to maintain, in our day, the dignity and usefulness of a profession which has included in it so many good and illustrious men, and which has for so many centuries been one of the foremost branches of intellectual activity.The foundations of medical science have been laid in an antiquity beyond the reach of historical investigation; its terms are the monuments of forgotten theories; in its progress, it has reflected the myriad aspects of hluman thought ; to its storehouses of knowledge, all civilised nations have borne their contributions.If, in its course of development, it has shared the errors and shlortcomings which are inseparable from human progress, none the less have its advances been fairly abreast of those made in other branches of knowled(ge.I have no fear but that this will con- tinue to be so, and that as medicine is, and must be, one of the most beneficial, it will also remain one of thle most liberal and enlightened of professions.
Association between patient-reported outcomes (PROs) and changes in prostate-specific antigen (PSA) in patients (pts) with advanced prostate cancer treated with apalutamide (APA) in the SPARTAN and TITAN studies.
Authors: Eric Jay Small, Kim N. Chi, Simon Chowdhury, Katherine B. Bevans, Amitabha Bhaumik, Fred Saad, Byung Chung, Lawrence Ivan Karsh, Stephane Oudard, Peter De Porre, Sabine D. Brookman-May, Sharon Anne McCarthy, Suneel Mundle, Hirotsugu Uemura, Matthew Raymond Smith, Neeraj Agarwal
Journal: Journal of Clinical Oncology (2022)

73 Background: In phase 3 placebo (PBO)-controlled studies, addition of APA to androgen deprivation therapy (ADT) improved overall survival, resulted in rapid and deep PSA declines, and reduced risk of disease progression while preserving health-related quality of life (HRQoL) in nonmetastatic castration-resistant prostate cancer (nmCRPC; SPARTAN) and metastatic castration-sensitive prostate cancer (mCSPC; TITAN). This post hoc analysis evaluated the association of a deep PSA decline with PROs in these studies. Methods: Pts on ADT were randomized to APA (240 mg QD) or PBO: SPARTAN 2:1 (N = 1,207; APA n = 806), TITAN 1:1 (N = 1,052; APA n = 525). Each cycle was 28 d. PROs were assessed using Functional Assessment of Cancer Therapy-Prostate (FACT-P), Brief Pain Inventory-Short Form (BPI-SF; TITAN only), and Brief Fatigue Inventory (BFI; TITAN only) at baseline, specific cycles during study treatment, and post progression up to 1 yr. A landmark analysis at Month 3 evaluated association between deep PSA decline (≤ 0.2 ng/mL) and time to subsequent deterioration in PROs (defined as decrease ≥ 10 points FACT-P total, ≥ 3 points Physical Wellbeing, ≥ 30% baseline for BPI-SF worst pain, or ≥ 2 points for BFI worst fatigue). At time of the landmark analysis, only pts continuing treatment were included; all deep PSA responses after, and all PRO deterioration events before, were ignored. Time-to-event end points were analyzed by Kaplan-Meier method and Cox proportional hazards model. Results: Median treatment durations were 32.9 mo (SPARTAN) and 39.3 mo (TITAN). Per assessment, &gt; 90% (SPARTAN, cycles 1-81) and &gt; 50% (TITAN, cycles 1-33) of eligible pts completed FACT-P; BPI-SF and BFI, both &gt; 62% (TITAN, cycles 1-33). Pts in either study who achieved PSA ≤ 0.2 ng/mL at Month 3 had a lower risk of deterioration in FACT-P total or Physical Wellbeing (Table). Pts in TITAN with PSA ≤ 0.2 ng/mL at Month 3 had a lower risk of BPI-SF worst pain intensity or BFI worst fatigue intensity progression (Table). Conclusions: Deep and rapid PSA responses with APA were associated with prolonged time to deterioration in HRQoL, FACT-P Physical Wellbeing, BPI-SF worst pain intensity, and BFI worst fatigue intensity in pts with advanced PC. Clinical trial information: NCT02489318 (TITAN); NCT01946204 (SPARTAN). [Table: see text]
Effects of naloxone on pethidine-induced neonatal depression. Part I--Intravenous naloxone.
Authors: P C Wiener, M I Hogg, M Rosen
Journal: BMJ (1977)

Infants whose mothers had had pethidine during labour were given either naloxone 40 microgram or isotonic saline administered intravenously double-blind within one minute of birth. Peak alveolar carbon dioxide tension, carbon dioxide excretion, alveolar ventilation, feeding behaviour, and habituation to a specific sound stimulus were measured regularly up to 48 hours after birth. Alveolar carbon dioxide tension was significantly lower and alveolar ventilation significantly higher half an hour after birth in the naloxone-treated group than in the saline-treated group, but these differences between the groups were not significant at any other time, and there were no significant differences in sucking frequency or pressure, milk consumption, or habituation to the auditory stimulus.
Association between recombinant human erythropoietin and quality of life and exercise capacity of patients receiving haemodialysis. Canadian Erythropoietin Study Group.
Authors: Andreas Laupacis, E Williams, L Jones, P Vessey, K Mcpherson
Journal: BMJ (1990)

OBJECTIVE--To determine whether recombinant human erythropoietin improves the quality of life and exercise capacity of anaemic patients receiving haemodialysis. DESIGN--A double blind, randomised, placebo controlled study. SETTING--Eight Canadian university haemodialysis centres. PATIENTS--118 Patients receiving haemodialysis aged 18-75 with haemoglobin concentrations less than 90 g/l, no causes of anaemia other than erythropoietin deficiency, and no other serious diseases. INTERVENTIONS--Patients were randomised to three groups to receive placebo (n = 40), erythropoietin to achieve a haemoglobin concentration of 95-110 g/l (n = 40), or erythropoietin to achieve a haemoglobin concentration of 115-130 g/l (n = 38). Erythropoietin was given intravenously thrice weekly, initially at 100 units/kg/dose. The dose was subsequently adjusted to achieve the target haemoglobin concentration. All patients with a serum ferritin concentration less than 250 micrograms/l received oral or intravenous iron for one month before the study and as necessary throughout the trial. MAIN OUTCOME MEASURES--Scores obtained with kidney disease questionnaire, sickness impact profile, and time trade off technique; and results of six minute walk test and modified Naughton stress test. RESULTS--The mean (SD) haemoglobin concentration at six months was 74 (12) g/l in patients given placebo, 102 (10) g/l in those in the low erythropoietin group, and 117 (17) g/l in those in the high erythropoietin group. Compared with the placebo group, patients treated with erythropoietin had a significant improvement in their scores for fatigue, physical symptoms, relationships, and depression on the kidney disease questionnaire and in the global and physical scores on the sickness impact profile. The distance walked in the stress test increased in the group treated with erythropoietin, but there was no improvement in the six minute walk test, psychosocial scores on the sickness impact profile, or time trade off scores. There was no significant difference in the improvement in quality of life or exercise capacity between the two groups taking erythropoietin. Patients taking erythropoietin had a significantly increased diastolic blood pressure despite an increase in either the dose or number of antihypertensive drugs used. Eleven of 78 patients treated with erythropoietin had their sites of access clotted compared with only one of 40 patients given placebo. CONCLUSIONS--Patients receiving erythropoietin were appreciably less fatigued, complained of less severe physical symptoms, and had moderate improvements in exercise tolerance and depression compared with patients not receiving erythropoietin. At the doses used in this trial there was a higher incidence of hypertension and clotting of the vascular access in patients treated with erythropoietin.
Long noncoding RNA LINC01234 promotes hepatocellular carcinoma progression through orchestrating aspartate metabolic reprogramming
Authors: Muhua Chen, Chunfeng Zhang, Wei Liu, Xiaojuan Du, Xiaofeng Liu, Baocai Xing
Journal: Molecular Therapy (2022)

Amino acids metabolism, especially aspartate metabolism, is often altered in human cancers including hepatocellular carcinoma (HCC) and this metabolic remodeling is required for supporting cancer cell malignant activities. Argininosuccinate synthase 1 (ASS1), as a crucial rate-limiting enzyme in aspartate metabolism, participates in repressing tumor progression. However, the roles of long noncoding RNAs (lncRNAs) in aspartate metabolism remodeling and the underlying mechanisms remain unclear. Here, we screen LINC01234 as an aspartate metabolism-related lncRNA in HCC. Clinically, LINC01234 was highly expressed in HCC, and a high LINC01234 expression level was correlated with a poor prognosis of patients with HCC. LINC01234 promoted cell proliferation, migration, and drug resistance by orchestrating aspartate metabolic reprogramming in HCC cells. Mechanistically, LINC01234 downregulated the expression of ASS1, leading to am increased aspartate level and activation of the mammalian target of rapamycin pathway. LINC01234 bound to the promoter of ASS1 and inhibited transcriptional activation of ASS1 by transcriptional factors, including p53. Finally, inhibiting LINC01234 dramatically impaired tumor growth in nude mice and sensitized HCC cells to sorafenib. These findings demonstrate that LINC01234 promotes HCC progression by modulating aspartate metabolic reprogramming and might be a prognostic or therapeutic target for HCC. Amino acids metabolism, especially aspartate metabolism, is often altered in human cancers including hepatocellular carcinoma (HCC) and this metabolic remodeling is required for supporting cancer cell malignant activities. Argininosuccinate synthase 1 (ASS1), as a crucial rate-limiting enzyme in aspartate metabolism, participates in repressing tumor progression. However, the roles of long noncoding RNAs (lncRNAs) in aspartate metabolism remodeling and the underlying mechanisms remain unclear. Here, we screen LINC01234 as an aspartate metabolism-related lncRNA in HCC. Clinically, LINC01234 was highly expressed in HCC, and a high LINC01234 expression level was correlated with a poor prognosis of patients with HCC. LINC01234 promoted cell proliferation, migration, and drug resistance by orchestrating aspartate metabolic reprogramming in HCC cells. Mechanistically, LINC01234 downregulated the expression of ASS1, leading to am increased aspartate level and activation of the mammalian target of rapamycin pathway. LINC01234 bound to the promoter of ASS1 and inhibited transcriptional activation of ASS1 by transcriptional factors, including p53. Finally, inhibiting LINC01234 dramatically impaired tumor growth in nude mice and sensitized HCC cells to sorafenib. These findings demonstrate that LINC01234 promotes HCC progression by modulating aspartate metabolic reprogramming and might be a prognostic or therapeutic target for HCC.
IMPACT OF ANGIOGRAPHIC COMPLETE REVASCULARIZATION AFTER DRUG-ELUTING STENT IMPLANTATION OR CORONARY ARTERY BYPASS SURGERY FOR MULTIVESSEL CORONARY DISEASE
Authors: Young-Hak Kim, Yong-Giun Kim, Gyung-Min Park, Ki Won Hwang, Chang Hoon Lee, Jung-Min Ahn, Hae Geun Song, Won-Jang Kim, Jong-Young Lee, Soo-Jin Kang, Duk-Woo Park, Seung-Whan Lee, Cheol Whan Lee, Seong-Wook Park, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2011)
Intestinal Diverticula
Authors: J. K. McCollum
Journal: BMJ (1959)

The possibility of her being a chimera appeared unlikely because of the variable reactions with anti-B sera and the apparent absence of signs of heterogeneity for any of the other blood-group systems.Investiga- tions of the patient herself were cut short by her death E few weeks after they began.Genetical Study An investigation of the family put a completely different complexion upon the case.Fortunately a number of relatives were available and proved most co-operative.Their blood groups are shown in the pedigree.In the case of the ABO, Rh, and MNS &A,B(A8) X Aa O(00) , A1 CcDec(CDelcde) CcDEe(CDe/cDE) Ccddee(Cde/cde) Ccddee(Cde/cd) ccddee(cde/cde) NNss(NsNs) NNS(NSNs) MNS(MSNs) NNS MNS ,_pi ,P P,+ P-PI,-
Questions and Answers
Journal: JAMA (1979)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
LEFT VENTRICULAR EJECTION FRACTION MEASURED WITH SAME DAY 2D ECHOCARDIOGRAPHY AND CMR IN PATIENTS WITH SUSPECTED CARDIOTOXICITY
Authors: Muhummad Sohaib Nazir, Maria Sol Andres, Theodore Murphy Sivatharshini Ramalingham, Resham Baurah, Stuart D. Rosen, Amedeo Chiribiri, Sven Plein, Sanjay Prasad, Raad Mohiaddin, Rajdeep Khattar, A John Baksi, Alexander Lyon
Journal: JACC CardioOncology (2022)
3. Prevention or Delay of Type 2 Diabetes: <i>Standards of Medical Care in Diabetes—2020</i>
Journal: Diabetes Care (2019)

The American Diabetes Association (ADA) “Standards of Medical Care in Diabetes” includes the ADA’s current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee (https://doi.org/10.2337/dc20-SPPC), are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA’s clinical practice recommendations, please refer to the Standards of Care Introduction (https://doi.org/10.2337/dc20-SINT). Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.
Prevalence and natural history of non-metastatic castrate resistant prostate cancer: A population-based analysis.
Authors: Amanda Elizabeth Hird, Erind Dvorani, Refik Saskin, Sender Herschorn, Ronald Kodama, Girish S. Kulkarni, Robert Nam
Journal: Journal of Clinical Oncology (2022)

65 Background: The natural history of non-metastatic castrate resistant prostate cancer (nmCRPC) prior to the introduction of novel anti-androgen agents in a real-world setting is largely unknown. Methods: This was a retrospective population-based cohort study of men with nmCRPC in Ontario, Canada. Patients with a diagnosis of prostate cancer, castrate level of testosterone ( &lt; 1.7nmol/L) and a PSA &gt; 2.0nmol/L with a subsequent rise &gt; 25% from the nadir, and without diagnostic or treatment codes for metastasis were included. Annual prevalence of nmCRPC was calculated. Crude time from nmCRPC to metastasis and death are presented as medians with interquartile range (IQR). Predictors of time from nmCRPC to prostate cancer death were compared using univariable and multivariable Fine and Gray subdistributional hazard models to account for the competing risk of non-prostate cancer death. Results: From January 2007 until March 2018, we identified 2045 patients with nmCRPC. Median age was 79 years (IQR: 72-84). A total of 984 patients (48.1%) received upfront hormonal therapy while 584 (25.8%) received initial radiotherapy (RT) and 478 (23.4%) underwent radical prostatectomy. Median time from primary treatment to nmCRPC was 6 years (IQR: 3-10). PSA at the time of meeting nmCRPC criteria was a median of 3.0 ng/L. Patients were followed for a median 31.1 months (IQR: 19.8-47.9). The overall annual prevalence of nmCRPC ranged from 1,519-1,913 patients, representing 7-12% of men with prostate cancer prescribed androgen deprivation therapy each year. Crude median time from nmCRPC to all-cause death was 37.6 months (IQR: 22.1-55.4). Median time from nmCRPC to metastasis and metastasis to all-cause death was 20.0 and 8.3 months, respectively. On regression analysis, older age, ADT use with primary treatment, higher PSA at the time of meeting nmCRPC criteria, and grade group predicted time from nmCRPC to prostate cancer death. Conclusions: This is the largest analysis of the prevalence and natural history of nmCRPC. The current study can be used as a historical cohort to compare how novel imaging modalities and advancements in systemic therapy for patients with nmCRPC impact prevalence estimates and disease trajectory over time.