Exploring the use of ChatGPT in predicting anterior circulation stroke functional outcomes after mechanical thrombectomy: a pilot study.

BACKGROUND: Accurate prediction of functional outcomes is crucial in stroke management, but this remains challenging. OBJECTIVE: To evaluate the performance of the generative language model ChatGPT in predicting the functional outcome of patients with acute ischemic stroke (AIS) 3 months after mechanical thrombectomy (MT) in order to assess whether ChatGPT can used to be accurately predict the modified Rankin Scale (mRS) score at 3 months post-thrombectomy. METHODS: We conducted a retrospective analysis of clinical, neuroimaging, and procedure-related data from 163 patients with AIS undergoing MT. The agreement between ChatGPT's exact and dichotomized predictions and actual mRS scores was assessed using Cohen's κ. The added value of ChatGPT was measured by evaluating the agreement of predicted dichotomized outcomes using an existing validated score, the MT-DRAGON. RESULTS: ChatGPT demonstrated fair (κ=0.354, 95% CI 0.260 to 0.448) and good (κ=0.727, 95% CI 0.620 to 0.833) agreement with the true exact and dichotomized mRS scores at 3 months, respectively, outperforming MT-DRAGON in overall and subgroup predictions. ChatGPT agreement was higher for patients with shorter last-time-seen-well-to-door delay, distal occlusions, and better modified Thrombolysis in Cerebral Infarction scores. CONCLUSIONS: ChatGPT adequately predicted short-term functional outcomes in post-thrombectomy patients with AIS and was better than the existing risk score. Integrating AI models into clinical practice holds promise for patient care, yet refining these models is crucial for enhanced accuracy in stroke management.

Successful Treatment of a Child With Epileptic Encephalopathy With Spike-Wave Activation in Sleep and GRIN2A Variant Using Sulthiame.

Epileptic encephalopathy with spike-wave activation in sleep (EE-SWAS) and developmental EE-SWAS (DEE-SWAS) are characterized by variable combinations of cognitive, language, behavioral, and/or motor regression associated with continuous or near-continuous diffuse spike-and-wave complexes during sleep. Glutamate ionotropic receptor NMDA type subunit 2A (GRIN2A) variants have been associated with EE-SWAS. It encodes the most relevant GluN2 subunit of the N-methyl-D-aspartate receptor (NMDAR). Sulthiame reduces NMDAR-mediated neuronal excitability and has been progressively used as monotherapy in self-limited epilepsy with centrotemporal spikes (SeLECTS) or as add-ontherapy in EE-SWAS/DEE-SWAS. A five-year-old female, with family history of epilepsy, was initially diagnosed with SeLECTS and medicated with valproic acid (VPA). One year later, she presented a focal to bilateral tonic-clonic seizure during sleep and learning difficulty. The electroencephalogram revealed continuous spike-and-wave during sleep leading to the diagnosis of EE-SWAS. Prednisolone was effective, but there was repeated recurrence after its discontinuation and associated adverse effects. As an alternative, sulthiame was added to VPA. Four years later, she remains clinically stable. Genetic testing revealed a GRIN2A missense variant, C.3228C>A (p.Asn1076Lys). Sulthiame appeared effective in this recurrent EE-SWAS child, who presented a GRIN2A missense variant with possible NMDAR gain-of-function and adverse effects of corticosteroids. Functional studies​​​​​​​ of GRIN2A variants might become a future tool for individualized therapies.

Persistent headache attributed to past cervicocephalic artery dissection: clinical characteristics and contributors to headache persistence.

BACKGROUND: Persistent headache/facial/neck pain attributed to past cervicocephalic arterial dissection is under-documented in literature. Our main goal was to evaluate clinical characteristics and contributors to this persistence. METHODS: A retrospective cohort study which included patients with a radiologically confirmed cervicocephalic arterial dissection (2015-2020) in a Portuguese tertiary hospital. Headache persistence was identified through clinical records. A questionnaire aimed to characterize headache in three moments: previous, persistent, and headache at the time of the interview (on average 2.5 years post-event). RESULTS: Ninety-two patients were identified; 24 (26.1%) had headache persistence ≥3 months, and 20 (22.2%) on average after 2.5 years post-event. There were no differences regarding demographics and vascular risk factors among patients with (n = 22) and without (n = 68) headache persistence. The first group had higher previous headache history (68.2% vs 4.4%, p < 0.001), delay in diagnosis (3.6 vs 1.9 days, p < 0.001), and headache/cervicalgia as the first symptom (81.8% vs 41.2%, p < 0.001). At the time of the interview, 20% still reported daily headache. A logistic regression model depicted headache history (OR = 59.8, p < 0.001), acute headache/cervicalgia (odds ratio, OR = 25.4, p = 0.005), posterior circulation dissection (OR = 7.6, p < 0.001), and less than 4 points by National Institutes of Health Stroke Scale score (OR = 5.0, p = 0.025) as contributors to headache persistence. CONCLUSION: Headache persistence post-cervicocephalic arterial dissection is common, and frequently affects patients daily. As it potentially affects functional outcomes and quality of life, the contributors identified in this study may help clinicians manage patients after the acute event.

Pituitary Adenoma "Pneumo-Apoplexy".

Tension pneumosella has been recognized as a very rare complication of pituitary transsphenoidal surgery. To the best of our knowledge, we report the second case of a pituitary adenoma "pneumo-apoplexy", which is characterized by findings consistent with tension pneumosella in the context of apoplexy of a pituitary adenoma; although it is an extremely rare diagnosis, it should be considered in patients with compatible clinical and radiological findings, particularly with a previous history of transsphenoidal pituitary surgery.

Multiple Sclerosis in rheumatic patients treated with tumor necrosis factor alpha inhibitors: a single-center retrospective case series and literature review.

Tumor necrosis factor alpha inhibitors (TNFi) are basilar treatments in a number of inflammatory rheumatic conditions and autoimmune phenomena such as de novo neuroinflammatory events were already described in these populations under TNFi. We conducted a single-center retrospective study in a cohort of rheumatic patients treated with TNFi to characterize neurological demyelinating/inflammatory disease in these patients. We report 3 cases (n= 744): all of them had spondyloarthritis, the onset of neurological manifestations occurred between 37 and 58 years old and all of them initially presented with an optic neuritis. The neurological symptoms emerged between 13 and 26 months after starting TNFi. All patients discontinued treatment with TNFi, but one resumed therapy with symptomatic worsening, having to interrupt treatment again. All patients, latter on, fulfilled multiple sclerosis (MS) McDonald criteria 1 and were diagnosed with relapsing-remitting MS. Our study support the prior view of a risk, disease-dependent or agent-dependent, although a causal relationship is yet to be enlightened.

The Future of Telemedicine in the Management of Heart Failure Patients.

Telemedicine (TM) is potentially a way of escalating heart failure (HF) multidisciplinary integrated care. Despite the initial efforts to implement TM in HF management, we are still at an early stage of its implementation. The coronavirus disease 2019 pandemic led to an increased utilisation of TM. This tendency will probably remain after the resolution of this threat. Face-to-face medical interventions are gradually transitioning to the virtual setting by using TM. TM can improve healthcare accessibility and overcome geographic inequalities. It promotes healthcare system efficiency gains, and improves patient self-management and empowerment. In cooperation with human intervention, artificial intelligence can enhance TM by helping to deal with the complexities of multicomorbidity management in HF, and will play a relevant role towards a personalised HF patient approach. Artificial intelligence-powered/telemedical/heart team/multidisciplinary integrated care may be the next step of HF management. In this review, the authors analyse TM trends in the management of HF patients and foresee its future challenges within the scope of HF multidisciplinary integrated care.

Contralateral Axillary Lymph Node Metastasis in a Patient with Relapsed Breast Cancer: Locoregional Event or Distant Metastasis Disease?

INTRODUCTION: Contralateral axillary lymph node metastasis (CAM) is a rare clinical condition in patients with breast cancer. It can be explained from hematogenous spread from the original primary tumor (stage IV) to aberrant regional lymphatic drainage to the contralateral axilla. However, according to the current clinical guidelines, regardless of its origin, CAM is considered as metastatic disease. CASE PRESENTATION: A 68-year-old woman presented with relapsed right breast cancer; lymphoscintigraphy showed only one sentinel lymph node (SLN) in the contralateral axilla (left region). Twenty-four hours later, the patient underwent upper internal quadrantectomy and bilateral selective lymph node biopsy. The final pathological analysis revealed one contralateral macrometastasis (>4 mm) in one left SLN. Subsequently, second-level left lymphadenectomy was performed. Currently the patient is being treated with chemotherapy, with appropriate clinical response. DISCUSSION: Our patient was considered to be node-positive rather than having metastatic disease since the preoperative lymphoscintigraphy demonstrated contralateral lymphatic drainage. Through preoperative scan in patients with relapsed breast cancer with clinically negative lymph nodes and CAM, it is possible to identify those cases that would benefit from therapy with curative intention.

Papel de la desnutrición en la síntesis de colágeno en anastomosis cólicas primarias: análisis de procolágeno y telopéptido carboxiterminal mediante radioinmunoanálisis / Role of malnutrition in collagen synthesis in primary colonic anastomosis. Analysis of procollagen and carboxyterminal telopeptide through radioimmunoassay

Introducción: Diversos factores clínicos, anatomopatológicos y técnicos influyen en la cicatrización correcta de las suturas intestinales tras la práctica de una resección intestinal. Uno de los factores más implicados es el estado nutricional del paciente. Objetivos: Evaluar la influencia de la desnutrición inducida en la viabilidad de una anastomosis intestinal primaria mediante el análisis del procolágeno (PINP) y del telopétido carboxiterminal del colágeno I (ICTP) depositados en ella. Material y método: Usamos 40 ratas Wistar y material de radioinmunoanálisis (kits comerciales de RIA ICTP-RIA® e Intact PINP®). Se formaron 2 grupos de ratas, 20 animales para cada grupo: grupo control (A) y grupo "desnutrición" (B). Se analizó PINP e ICTP mediante RIA sobre tejido colónico homogeneizado, preanastomótico y anastomótico. Resultados: Hay menores valores de PINP en el colon de las ratas del grupo B que en el del grupo A (0,3620 y 0,4340 µg/g, respectivamente) (p = 0,032). Hay un mayor valor de ICTP analizado en el colon del grupo B (0,9545 en contraposición a 0,8460 µg/g, en el grupo A) (p = 0,875). En las anastomosis del grupo B hay menos síntesis de PINP que en el grupo A (0,376 y 0,468 µg/g, respectivamente; p = 0,002). Conclusiones: La anastomosis colónica incrementa las concentraciones de PINP e ICTP en el tejido cicatrizal (p < 0,001); la desnutrición reduce la colagenización de las anastomosis (p < 0,001)

Introduction: Various clinical, pathological and technical factors influence the viability of intestinal suturing after intestinal resection. One of the most important factors is the patient's nutritional status. Objectives: To evaluate the influence of induced nutrition on the viability of primary intestinal anastomosis by means of analysis of collagen I procollagen (PINP) and telopeptide (ICTP) deposited in the anastomosis. Material and method: 40 Wistar rats and material for the radioimmunoassay (ICTP-RIA® and Intact PINP® commercial radioimmunoassay kits) were used. We used two groups of 20 rats each: control group (A) and a "malnourished" group (B). PINP and ICTP were analyzed through radioimmunoassay of homogenized, preanastomotic and anastomotic colonic tissue. Results: PINP levels were lower in the colons of group B rats than in the control group (0.3620 and 0.4340 µg/g respectively) (p = 0.032). ICTP levels were higher in the colons of group B rats than in those of group A rats (0.9545 versus 0.8460 µg/g respectively) (p = 0.875). PINP synthesis was lower in the anastomoses of group B than in group A (0.376 and 0.468 µg/g respectively; p = 0.002). Conclusions: Colonic anastomosis increases PINP and ICTP levels in scar tissue (p < 0.001). Malnutrition reduces collagenization of colonic anastomoses (p < 0.001)

Aplidin induces apoptosis in human cancer cells via glutathione depletion and sustained activation of the epidermal growth factor receptor, Src, JNK, and p38 MAPK.

We report that Aplidin, a novel antitumor agent of marine origin presently undergoing Phase II clinical trials, induced growth arrest and apoptosis in human MDA-MB-231 breast cancer cells at nanomolar concentrations. Aplidin induced a specific cellular stress response program, including sustained activation of the epidermal growth factor receptor (EGFR), the non-receptor protein-tyrosine kinase Src, and the serine/threonine kinases JNK and p38 MAPK. Aplidin-induced apoptosis was only partially blocked by the general caspase inhibitor benzyloxycarbonyl-VAD-fluoromethyl ketone and was also sensitive to AG1478 (an EGFR inhibitor), PP2 (an Src inhibitor), and SB203580 (an inhibitor of JNK and p38 MAPK) in MDA-MB-231 cells. Supporting a role for EGFR in Aplidin action, EGFR-deficient mouse embryo fibroblasts underwent apoptosis upon treatment more slowly than wild-type EGFR fibroblasts and also showed delayed JNK and reduced p38 MAPK activation. N-Acetylcysteine and ebselen (but not other antioxidants such as diphenyleneiodonium, Tiron, catalase, ascorbic acid, and vitamin E) reduced EGFR activation by Aplidin. N-Acetylcysteine and PP2 also partially inhibited JNK and p38 MAPK activation. The intracellular level of GSH affected Aplidin action; pretreatment of cells with GSH or N-acetylcysteine inhibited, whereas GSH depletion caused, hyperinduction of EGFR, Src, JNK, and p38 MAPK. Remarkably, Aplidin also induced apoptosis and activated EGFR, JNK, and p38 MAPK in two cell lines (A-498 and ACHN) derived from human renal cancer, a neoplasia that is highly refractory to chemotherapy. These data provide a molecular basis for the anticancer activity of Aplidin.

Aplidin induces the mitochondrial apoptotic pathway via oxidative stress-mediated JNK and p38 activation and protein kinase C delta.

Aplidin, a new antitumoural drug presently in phase II clinical trials, has shown both in vitro and in vivo activity against human cancer cells. Aplidin effectively inhibits cell viability by triggering a canonical apoptotic program resulting in alterations in cell morphology, caspase activation, and chromatin fragmentation. Pro-apoptotic concentrations of Aplidin induce early oxidative stress, which results in a rapid and persistent activation of both JNK and p38 MAPK and a biphasic activation of ERK. Inhibition of JNK and p38 MAPK blocks the apoptotic program induced by Aplidin demonstrating its central role in the integration of the cellular stress induced by the drug. JNK and p38 MAPK activation results in downstream cytochrome c release and activation of caspases -9 and -3 and PARP cleavage, demonstrating the mediation of the mitochondrial apoptotic pathway in this process. We also demonstrate that protein kinase C delta (PKC-delta) mediates the cytotoxic effect of Aplidin and that it is concomitantly processed and activated late in the apoptotic process by a caspase mediated mechanism. Remarkably, cells deficient in PKC-delta show enhanced survival upon drug treatment as compared to its wild type counterpart. PKC-delta thus appears as an important component necessary for full caspase cascade activation and execution of apoptosis, which most probably initiates a positive feedback loop further amplifying the apoptotic process.