Prediction of Prednisolone Dose Correction Using Machine Learning.

Wrong dose, a common prescription error, can cause serious patient harm, especially in the case of high-risk drugs like oral corticosteroids. This study aims to build a machine learning model to predict dose-related prescription modifications for oral prednisolone tablets (i.e., highly imbalanced data with very few positive cases). Prescription data were obtained from the electronic medical records at a single institute. Cluster analysis classified the clinical departments into six clusters with similar patterns of prednisolone prescription. Two patterns of training datasets were created with/without preprocessing by the SMOTE method. Five ML models (SVM, KNN, GB, RF, and BRF) and logistic regression (LR) models were constructed by Python. The model was internally validated by five-fold stratified cross-validation and was validated with a 30% holdout test dataset. Eighty-two thousand five hundred fifty-three prescribing data for prednisolone tablets containing 135 dose-corrected positive cases were obtained. In the original dataset (without SMOTE), only the BRF model showed a good performance (in test dataset, ROC-AUC:0.917, recall: 0.951). In the training dataset preprocessed by SMOTE, performance was improved on all models. The highest performance models with SMOTE were SVM (in test dataset, ROC-AUC: 0.820, recall: 0.659) and BRF (ROC-AUC: 0.814, recall: 0.634). Although the prescribing data for dose-related collection are highly imbalanced, various techniques such as the following have allowed us to build high-performance prediction models: data preprocessing by SMOTE, stratified cross-validation, and BRF classifier corresponding to imbalanced data. ML is useful in complicated dose audits such as oral prednisolone. Supplementary Information: The online version contains supplementary material available at 10.1007/s41666-023-00128-3.

Prevention of intubation-induced mucosal damage using a tube coated with 2-methacryloyloxyethyl phosphorylcholine polymer.

BACKGROUND AND OBJECTIVE: Tracheal intubation is associated with various complications that include epithelial injury. Abrasion of the fragile tracheal epithelium can occur at the points of contact between the tube and mucosa subject to respiratory movement. In this original experiment, we examined the mucosal protective effect of coating endotracheal tubes with poly[2-methacryloyloxyethl phosphorylcholine (MPC)-co-n-butyl methacrylate] (PMB). METHODS: We prepared four types of tubes: tube A (control, no coating), tube B (two coats, 0.5% PMB), tube C (10 coats, 0.5% PMB) or tube D (one coat, 5% PMB). Twenty-nine beagle dogs were divided into four groups and orally intubated with tube A, B, C or D for 4±0.5 h. The cuffs of extubated tubes were stained with haematoxylin. Paraffin sections from tracheal walls in contact with the inflated cuff were stained with haematoxylin/eosin and periodic acid-Schiff. RESULTS: Cuffs of tubes A and B were strongly stained with haematoxylin because of attached epithelial cells. Stained areas in those of tubes C and D were significantly reduced. Histological analysis showed that a single coat of 5% PMB prevented epithelial abrasion and proliferation of goblet cells. Excess tracheal mucus was observed in the tube A group, but not in the tube D group. CONCLUSION: Tracheal epithelial damage caused by intubation was greatly reduced or eliminated by PMB coating on the surface of the tracheal tube.

Cellulose acetate beads activate the complement system but inactivate the anaphylatoxins generated.

The generation of anaphylatoxins, particularly C5a, is important in extracorporeal circulation therapies such as granulocyte/monocyte apheresis, which activates the complement system and elevates C5a levels. However, no side effects of granulocyte/monocyte apheresis using cellulose acetate beads have been reported. To investigate the mechanism of complement activation, we prepared plasma from cellulose acetate bead-treated blood (P-CAB) and compared it with zymosan-activated plasma (ZAP). Anaphylaxis activity was measured by skin test, and the activity of carboxypeptidase, which inactivates C5a, was measured by colorimetric assay. Pro-carboxypeptidase R and neutrophil elastase concentrations were measured by enzyme-linked immunosorbent assay. Although C5a was generated in P-CAB, the anaphylaxis activity of P-CAB was lower than that of ZAP. Carboxypeptidase activity and pro-carboxypeptidase R levels were suppressed in P-CAB, but not in ZAP. Furthermore, neutrophil elastase levels increased in P-CAB. The decreases in carboxypeptidase activity and inactivation of anaphylatoxin were inhibited by a neutrophil elastase inhibitor. These results suggest that cellulose acetate beads initiate the activation of carboxypeptidase R via elastase release, thereby inducing the inactivation of anaphylatoxin.

Interleukin-6 induces prostaglandin E(2) synthesis in mouse astrocytes.

The physiological function of interleukin-6 within the central nervous system (CNS) is complex; interleukin-6 exerts neurotrophic and neuroprotective effects and yet can also function as a mediator of inflammation, demyelination, and astrogliosis depending on the cellular context. However, the roles of interleukin-6 in astrocytes are poorly understood. In the present study, we investigated the effect of the pro-inflammatory cytokine interleukin-6 on the production of the inflammatory mediator prostaglandin E(2) in mouse astrocytes. Interleukin-6 stimulated prostaglandin E(2) production in a time-dependent fashion via a rapid and transient induction of cyclooxygenase-2 messenger RNA, followed by cyclooxygenase-2 protein synthesis. Interleukin-6 may act on the nervous system by interacting with its specific soluble interleukin-6 receptor and the signal transducer 130-kDa glycoprotein. Simultaneous treatment of astrocytes with interleukin-6 and soluble interleukin-6 receptor caused marked induction of prostaglandin E(2) synthesis, and this effect was suppressed by adding a neutralizing antibody against soluble interleukin-6 receptor. Furthermore, the mouse 130-kDa glycoprotein antibody suppressed prostaglandin E(2) formation induced by interleukin-6, as well as interleukin-6/soluble interleukin-6 receptor complexes, in a dose-dependent manner. These results indicate that interleukin-6/soluble interleukin-6 receptor complexes and the signal transducer 130-kDa glycoprotein play an important role in the regulation of cyclooxygenase-2 expression and subsequent prostaglandin E(2) formation in mouse astrocytes and that interleukin-6 is an important regulator of immune and inflammatory processes in the CNS.

A case of a slipped medial rectus muscle after strabismus surgery.

BACKGROUND: A slipped muscle after strabismus surgery is a well known complication, but only a few cases have been reported in the medical literature. Here, we report a case of a slipped medial rectus muscle that occurred after strabismus surgery for esotropia. CASE REPORT: The patient was a 10 year old male with an acquired esotropia of 20 PD at distance. For treatment, 3.5 mm bilateral medial rectus recessions was performed. There were no complications during the procedure. On postoperative day 8, the eye position was orthotropic in primary position, but a right exotropia was observed in left gaze. The boy was frequently observed rubbing his right eye after surgery. The right exotropia increased to 30 PD 2 months after surgery. Limited adduction of the right eye, a large widening of the lid fissure on adduction, and mild exophthalmos were observed. Based on the above findings, a slipped medial rectus was suspected, and a second surgery, advancement of the right medial rectus muscle was performed 2.5 months after the initial procedure. After this second procedure, the eyes became orthotropic, and the adduction disorder, large widening the lid fissure, and mild exophthalmos resolved. CONCLUSION: The slipped muscle may have been caused by insufficient suture and/or excessive rubbing of the eye by the patient. When divergent strabismus is observed after recession of the medial rectus muscle, a slipped muscle should be considered as a differential diagnosis.

Treatment for A and V strabismus by slanting muscle insertions.

PURPOSE: To evaluate the therapeutic effects of surgically slanting extraocular muscle insertions. RESEARCH DESIGN: Observational case series. METHODS: We performed slanting recession and resection on medial or lateral rectus muscles. We created a slanting surgical reinsertion line with a 3-4 mm difference between upper and lower corners of the muscles, in 31 patients with A or V strabismus (V exotropia in 16 patients; A exotropia in 12; A esotropia in 3). Cases with V exotropia with moderate or marked overaction of inferior oblique muscle were excluded. RESULTS: V exotropia: The average amount of V pattern was 17.9 PD before and 7.6 PD after surgery. Slanting surgery reduced the V pattern in 15 of 16 patients. The mean amount of reduction was 10.3 PD in the V pattern and 29.8 PD in upgaze. A exotropia: The average amount of the A pattern was 26.6 PD before and 6.3 PD after surgery. Slanting surgery reduced the A pattern in 8 of 12 patients. The mean reduction was 20.3 PD in the A pattern and 36.4 PD in downgaze. A esotropia: The average amount of the A pattern was 23 PD before and 8 PD after surgery, reducing the A pattern in 1 of 3 patients. CONCLUSION: The surgical technique of slanting muscle insertions for correction of A and V strabismus is a suitable procedure for reducing or eliminating A and V patterns.

[Epidemic nosocomial keratoconjunctivitis caused by adenovirus type 4].

PURPOSE: To evaluate the clinical features of nosocomial epidemic keratoconjunctivitis(EKC) occurring in the ophthalmology ward of Sapporo Medical University Hospital and to devise preventive measures for it. MATERIALS AND METHODS: We studied the symptoms and clinical course of 2 patients who had EKC and 16 patients who had EKC caused by nosocomial infections in our hospital. We attempted to detect adenovirus antigen and viral DNA from conjunctival swabs and also to isolate the virus. RESULTS: The clinical symptoms of EKC were conjunctival hyperemia in 18 patients(100%), conjunctival follicles in 11 patients (61.1%), discharge in 8 patients(44.4%), superficial punctate keratopathy in 7 patients(38.9%), swelling of the eyelids in 3 patients(16.7%), and fever in 3 patients(16.7%). 72% were positive for Adeno-check. Adenovirus type 4 was isolated from the conjunctival swabs. We considered that the route of hospital infection was infection from the doctor's hands, from eye drops, and from contact lenses. We disclosed that nosocomical EKC had occurred in our hospital. The hospital infection was eliminated by closing the ophthalmology ward and sterilizing instruments and washing hands. CONCLUSIONS: The delay of proper measures increased the risk of nosocomical infection. We recognized the importance of careful observation of patients and immediate preventive efforts in nosocomical infection.