. * * window.aa needs to exist and be usable by ANY module's script, * however early it runs - main-nav's script, for one, runs near * the top of

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, well before the real search-insights.js * so the download * begins as early as before. Repeat calls share the same downloads, a * failed load is retried on the next call, and the versions / SRI * hashes live only here. * * Algolia Insights is unaffected: window.aa above is still created in * on every page and queues events until search-insights loads. * * window.loadAlgoliaLibs({ priority: 'high' }) (Oct 2026): used by the * /search page, where the first results wait on these libraries. Chrome * gives async scripts low priority, behind images and fonts; this asks * for high instead (fetchpriority). Only the first call for a library * sets its priority - later calls share that download. */ (function (win, doc) { var LIBS = [ { ready: function () { return !!win['algoliasearch/lite']; }, src: 'https://cdn.jsdelivr.net/npm/algoliasearch@5.52.1/dist/lite/builds/browser.umd.js', integrity: 'sha256-I2oYUIvhx1g6l4lTP+yoERbzLIHKzw4AKaBRQPwIeDY=' }, { ready: function () { return !!win.instantsearch; }, src: 'https://cdn.jsdelivr.net/npm/instantsearch.js@4.98.0/dist/instantsearch.production.min.js', integrity: 'sha256-ngmqZk4WBxUw257aMYZayyNBd983INngagv0jI6Ecfs=' } ]; function loadOne(lib, options) { if (lib.ready()) return Promise.resolve(); // One download per library, shared by every caller; reset on // failure so the next call retries just the library that failed. if (lib.pending) return lib.pending; lib.pending = new Promise(function (resolve, reject) { var script = doc.createElement('script'); script.src = lib.src; script.integrity = lib.integrity; script.crossOrigin = 'anonymous'; script.async = true; if (options && options.priority === 'high') script.setAttribute('fetchpriority', 'high'); script.onload = function () { lib.ready() ? resolve() : reject(new Error('Loaded but not available: ' + lib.src)); }; script.onerror = function () { script.remove(); reject(new Error('Could not load ' + lib.src)); }; doc.head.appendChild(script); }); lib.pending.catch(function () { lib.pending = null; }); return lib.pending; } win.loadAlgoliaLibs = function (options) { return Promise.all(LIBS.map(function (lib) { return loadOne(lib, options); })); }; })(window, document); . */ window.hsConversationsSettings = window.hsConversationsSettings || {}; window.hsConversationsSettings.loadImmediately = false; (function (win) { var EVENTS = ['pointerdown', 'keydown', 'touchstart', 'scroll', 'mousemove', 'wheel']; var done = false; /* 19 Oct 2026 - chat widget layout shift (field CLS). Phones fail Core Web Vitals on CLS (p75 ~0.2 site-wide in CrUX for months). Biggest cause found: HubSpot's chat container is fixed to the bottom-right corner and changes size - 100x96 launcher to 282x253 when the welcome message pops up (~5 s after load), and to full screen when a visitor opens the chat. Its top-left corner moves, so Chrome scores it as a layout shift: 0.088 per page view at 360x640 (0.044 at 412x850), on every page. Taps happen inside the chat iframe, so the parent page never sees the input and the open/close shifts count too. Fix: whenever the container's size changes it is made transparent for 400 ms (Chrome doesn't score shifts of invisible elements), then shown again at its new size. Tested on live io1001 at 360x640 in a cookie-less frame: the 0.088 shift no longer appears. The chat itself is unchanged - it just appears 0.4 s later at each resize. Relies on HubSpot's container id; if that changes this does nothing (no error). */ function cloakChatResizes() { var ID = 'hubspot-messages-iframe-container'; function watch(c) { if (c.getAttribute('data-bb-cloak')) return; c.setAttribute('data-bb-cloak', '1'); var last = c.offsetWidth + 'x' + c.offsetHeight, timer = null; new MutationObserver(function () { var size = c.offsetWidth + 'x' + c.offsetHeight; if (size === last) return; last = size; c.style.setProperty('opacity', '0', 'important'); clearTimeout(timer); timer = setTimeout(function () { c.style.removeProperty('opacity'); }, 400); }).observe(c, { attributes: true, attributeFilter: ['style', 'class'], subtree: true, childList: true }); } var found = document.getElementById(ID); if (found) { watch(found); return; } if (!document.body || !('MutationObserver' in win)) return; var mo = new MutationObserver(function () { var c = document.getElementById(ID); if (c) { mo.disconnect(); watch(c); } }); mo.observe(document.body, { childList: true }); setTimeout(function () { mo.disconnect(); }, 30000); } function loadWidget() { var api = win.HubSpotConversations; if (api && api.widget && api.widget.status && api.widget.status().loaded) return; try { cloakChatResizes(); } catch (e) {} if (api && api.widget) api.widget.load(); } function onFirstInteraction() { if (done) return; done = true; EVENTS.forEach(function (type) { win.removeEventListener(type, onFirstInteraction, { passive: true }); }); var start = function () { if (win.HubSpotConversations) loadWidget(); else (win.hsConversationsOnReady = win.hsConversationsOnReady || []).push(loadWidget); }; if ('requestIdleCallback' in win) win.requestIdleCallback(start, { timeout: 1500 }); else setTimeout(start, 200); } EVENTS.forEach(function (type) { win.addEventListener(type, onFirstInteraction, { passive: true }); }); })(window);

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Developing next-generation in vitro phenotypic assays for Huntington鈥檚 disease by combining a precision reprogrammed hiPSC-derived disease model with high-density microelectrode arrays
application note

Developing next-generation in vitro phenotypic assays for Huntington鈥檚 disease by combining a precision reprogrammed hiPSC-derived disease model with high-density microelectrode arrays

In this Application Note, Charles River Laboratories functionally characterised ioGlutamatergic Neurons HTT 50CAG/WT and ioGlutamatergic Neurons developed by 91探花 using the MaxTwo high-density microelectrode array from MaxWell Biosystems.
Developing next-generation in vitro phenotypic assays for Huntington鈥檚 disease by combining a precision reprogrammed hiPSC-derived disease model with high-density microelectrode arrays
In this Application Note, Charles River Laboratories functionally characterised ioGlutamatergic Neurons HTT 50CAG/WT and ioGlutamatergic Neurons developed by 91探花 using the MaxTwo high-density microelectrode array from MaxWell Biosystems.

Huntington鈥檚 disease (HD) is a fatal neurodegenerative disorder caused by the expansion of the CAG trinucleotide repeat in the huntingtin (HTT) gene leading to the expression of a mutant protein (mHTT), which affects neuronal health and function. There is currently no effective cure or treatment to slow down or stop the disease鈥檚 progression. One reason for this is the lack of accurate and easy-to use HD models that recapitulate the phenotypes and pathology seen in patients. Additionally, more advanced methods are required to record and analyze functional properties of cultured neurons over the entire maturation period, in order to gain insights into the underlying mechanisms of neurodegenerative diseases.

In this app note you will learn:

  • How Charles River Laboratories utilised the MaxTwo high-density microelectrode array from MaxWell Biosystems to functionally characterise the ioGluamatergic Neurons HTT50CAG/WT Huntington's disease model from 91探花.
  • How ioGlutamatergic Neurons HTT50CAG/WT and ioGlutamatergic Neurons form a genetically matched isogenic system that allows scientists to attribute experimental outcomes directly to the 50 CAG repeat expansion known to cause Huntington's disease.
  • How using the MaxTwo system, Charles River generated phenotypic data showing 91探花's Huntington's disease model has delayed neuronal network formation, decreased axonal branching and decreased spontaneous activity compared to the isogenic control.

 

91探花 | MaxWell Biosystems | Charles River Laboratories

2022

 

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