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Hamilton microsyringe

Manufactured by Hamilton Company
Sourced in United States, Switzerland, Germany

The Hamilton microsyringe is a precision instrument designed for accurate and controlled liquid handling. It features a high-quality glass barrel and a finely calibrated plunger for precise volume delivery. The microsyringe is suitable for a variety of laboratory applications that require the manipulation of small volumes of liquids.

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29 protocols using hamilton microsyringe

1

Subcutaneous Injections of ET-1 or NGF

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ET-1, NGF or its vehicle, were injected in a 10 µl volume subcutaneously (s.c.) into the mid-plantar hind paw, 1 cm distal from the heel, using a 30-G needle attached to a 10 µl Hamilton microsyringe (Hamilton Co., Reno, NV, USA). Injections occurred under brief general anesthesia with the inhalation of the rapidly reversible agent sevoflurane (Abbott Labs, N. Chicago, IL, USA).
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2

Bilateral Sulpiride Microinjection Dose Effects

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The D2R antagonist sulpiride (Sigma-Aldrich Co.: (S)-(−)-sulpiride, S7771) was bilaterally microinjected in three different doses: 0.1 μg, 1.0 μg, and 4.0 μg per side in 0.4 μl volume (0.73 mM, 7.32 mM, 29.29 mM, respectively). Controls received vehicle (0.4 μl). Thus, we had the 0.1D2anta, 1.0D2anta, 4.0D2anta and the control groups, respectively. sulpiride was dissolved in 0.1 N HCl, and after the addition of phosphate buffer it was titrated with 0.1 N NaOH. Control animals received vehicle (veh.) in equal volume to that used for the drug injections. The solutions were kept at + 4 °C before their applications. All the mentioned doses are meant to be the dose per side values. Stainless steel microinjection tubes extended 0.5 mm below the tips of the implanted guide cannulae. The delivery cannula was attached to a 10 µl Hamilton microsyringe (Hamilton Co., Bonaduz, Switzerland) via polyethylene tubing (PE-10). All injections were delivered by a syringe pump in the volume of 0.4 µl (Cole Parmer, IITC, Life Sci. Instruments, California) over a 60 s interval. After accomplishing the microinjection, the cannulae were left in place for 60 s to allow diffusion into the surrounding tissue. Rats were gently held by hand during the injection procedure.
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3

Modulating KCNQ1OT1 in Mouse Ischemic Stroke

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All experiments related to animals were approved by the Institutional Animal Care and Use Committee of China Medical University. This study was conducted in complete compliance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. We spared no effort to minimize the stress and pain of animals used in this trial. Male C57BL/6J mice weighing 22 to 25 g (8–10 weeks old) were provided by Beijing HFK Bioscience Cooperation, China. Mice were maintained in the standard environment of 22°C and 70% humidity in a 12 hr light/dark cycle, with access to food and water ad libitum. Lentivirus encoding short‐hairpin RNA targeting KCNQ1OT1 and its nontargeting sequence were used to infect mice brain tissue. Mice were divided into four groups (n = 10 per group): sham, tMCAO, tMCAO + sh‐NC, and tMCAO + sh‐KCNQ1OT1. LV3‐CMV‐GFPPuro‐sh‐KCNQ1OT1 or LV3‐CMV‐GFPPuro‐sh‐NC (5 µl of 108 TU/ml; GenePharma, Shanghai, China) was stereotaxically injected into the lateral ventricle via a Hamilton microsyringe (Hamilton Co., Reno, NV, USA) two weeks before tMCAO. The injection points were located anteroposterior (AP) −0.3 mm, mediolateral (ML) 1.00 mm, and dorsoventral (DV) −2.2 mm to the bregma.
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4

AAV2-Pim-1 Vector for Optic Nerve Repair

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The AAV2 virus packaging system consisted of pAOV-CAGMINI-eGFP, pAAV-RC and pHelper. Target gene Pim-1 was activated by promoter CAGMINI with neuro-specific expression. A pAOV-CAGMINI-eGFP-2A-Pim-1-3FLAG plasmid carrying the Pim-1(NM_017034) cDNA clone (Biostime Biotechnology Co., Shanghai, China) was used to produce AAV2-Pim-1. The positive PCR cloning was compared with that of the GenBank database; consistency of the comparison with the ID:NM_017034 indicated successful construction of the plasmid. Altogether 293 cells were transfected with the fluorescent protein eGFP expression plasmid through lipo2000, and the presence of green fluorescence 24 h after transfection indicated the successful transfection of AAV2-Pim-1 vector. Finally, AAV2-Pim-1 was packaged at AAV2-Pim-1 drop of 5.7×1012 vg/ml and AAV2-GFP drop of 3.57×1012 vg/ml, and stored at -80℃.
The experimental procedures were as follows: 5 µl Hamilton microsyringe (Hamilton Co., Switzerland) was used to inject 2 µl NS, AAV2-GFP and AAV2-Pim-1 in the left eye of the rat as designed. Four weeks after injection, a rat model of left optic nerve damage was established with a temporary mini-cerebral aneurysm clip, and then the left eye and optic nerve were removed and tested 2 weeks post injury.
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5

Lentiviral Injection into Lateral Ventricles

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Lentivirus (5 μL, 1 × 108 TU/mL) was injected into the lateral ventricles through a Hamilton microsyringe (Hamilton Co., Reno, NV, USA) 2 weeks before the surgical procedure. The detailed procedure was the same as that used in our previous study (Yu et al., 2019) and included cutting the skin and removing the local bone flap. A brain stereotaxic device was used to fix the injection site as follows: anteroposterior –0.3 mm, mediolateral 1.0 mm, and dorsoventral –2.2 mm.
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6

Injecting α-synuclein fibrils in mouse midbrain

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Mice were anesthetized for unilateral injections of WT α-syn fibrils or G51D α-syn fibrils (20 μg at 5 μg/μL) into the SNc using a Hamilton microsyringe (Hamilton Co, NV, USA) under stereotaxic surgery (1.3 mm lateral, −2.8 mm posterior from the bregma, 4.3 mm below the dural surface). At 12 or 24 weeks postinjection, fibrilinoculated mice were deeply anesthetized and perfused transcardially with 4% paraformaldehyde in PBS. The brains were removed, postfixed overnight in 4% paraformaldehyde in PBS, and immersed in PBS containing 30% sucrose until sinking.
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7

Intracerebral LPS Injection in Mice

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Ultra-pure LPS (Escherichia coli serotype 055:B5; Sigma, St. Louis, MO, USA) was dissolved in sterile saline at a concentration of 5 mg/ml. Mice were anesthetized by intraperitoneal injection of pentobarbital sodium (0.648 mg/10 g body weight) and placed into a rodent stereotaxic frame (David Kopf Instruments, Tujunga, CA, USA). The scalp was shaved and a burr hole was drilled 0.5 mm caudal to the bregma and 1.0 mm lateral to the midline. LPS (200 μg/kg) was injected via a Hamilton microsyringe (Hamilton Co., Reno, NV, USA) into the ventricle over a 5-min period. Sham animals received an isovolumetric ICV injection of saline.
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8

Investigating Roles of MEG3 and Sema3A in Mice MCAO

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Adult male C57BL/6J mice weighing 22 g -25 g were used for this study. Mice were allowed 1 week for adaption. The mice were arranged into four groups: the sham group, the MCAO group, the MCAO+si-MEG3 (intraventricular injection si-MEG3) group and the MCAO+si-MEG3+Sema3A group (intraventricular injection si-MEG3 and Sema3A). The methods for intraventricular injection were: i) mice were anesthetized with 10% chloral hydrate (3.2 ml/kg) by intraperitoneal injection and then placed on stereotactic frame; ii) si-MEG3 as well as si-MEG3+Sema3a were delivered to the right lateral ventricle through a Hamilton microsyringe (Hamilton Co., Reno, NV, USA); All experiments involving animals were in accordance with the institutional animal welfare guideline and approved by Institutional Animal Care and Use Committee of Qilu Hospital of Shandong University.
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9

Striatum Infusion of Excitotoxin in Rats

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Rats were deeply anesthetized with sodium pentobarbital (40 mg/kg, i.p.), placed in a stereotaxic equipment (Stoelting Co., Woo Dale, IL, USA) and administered in the right striatum with 1 μL of ISS or QUIN (equivalent to 120 or 240 nmol) using a 10 μL Hamilton microsyringe (Hamilton Co., Reno, NV, USA). The administration was carried out according the following stereotaxic coordinates: +0.5 mm anterior to bregma, -2.6 mm lateral to bregma and -4.5 mm ventral to dura [28] .
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10

Subcutaneous Injection of NGF and Inhibitors

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All injections were made subcutaneously (s.c.) into the mid-plantar surface of the hind paw, 1 cm distal from the heel using a 30-G needle attached to a 10 µl Hamilton microsyringe (Hamilton Co., Reno, NV, USA). The NGF-injected paw was identified as the Ipsilateral Paw (ILP) and the opposite paw as the Contralateral Paw (CLP). Injections occurred under brief general anesthesia caused by inhalation of the rapidly reversible agent sevoflurane (Abbott Labs, N. Chicago, IL, USA). Recovery of the righting reflex occurred in <30 sec after anesthesia inhalation was discontinued; 5–10 min later “normal” nocifensive responses to paw pinch could be assessed in control animals.
NGF, N-acetyl-D-sphingosine (C2-ceramide), GW4869, K252a or their vehicles, each were injected in 10 µl volumes, and antibodies to p75NTR or the TrkA receptor were injected in 20 µl volumes. The non-selective myristoylated pseudosubstrate inhibitor of atypical PKCs (mPSI- or “ZIP”; Standaert et al., 1997 (link)), or its inactive scrambled peptide homologue (scrambled ZIP), both at 40 µg/20 µl, were similarly injected, before NGF.
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