Search

Growth hormone may improve cardiac function in cases of heart failure resulting from dilated cardiomyopathy. Dilated cardiomyopathy refers to the enlargement of the left ventricle without appropriate thickening of the heart wall. Researchers gave growth hormone for three months to seven patients with dilated cardiomyopathy patients and moderate heart failure. Heart structure, blood flow, and exercise capacity was monitored before treatment, immediately after treatment, and three months after the end of treatment. Administration of growth hormone appeared to cause significant growth of heart muscle in the left-ventricular wall, improve the heart's pumping ability and efficiency, and increase the patient's exercise capacity. These effects were diminished but still apparent three months after treatment was stopped. The two-fold increase in the efficiency of the left ventricle that was observed following treatment might be explained by the reduced stress in a thicker heart wall.

The forearm perfusion method helps study the adrenergic mechanisms due to hypoglycemia, role of skeletal muscle in hypoglycemia and effect of insulin on muscle tissue sensitivity and indicates beta-adrenergic stimulation-induced resistance of skeletal muscle to insulin during hypoglycemia. This limited glucose intake by muscle tissues helps counteract hypoglycemia. The release of gluconeogenic substrates from muscles is poor and does not influence gluconeogenesis.

A study of the effect of reflex induction of Norepinephrine (NE) release due to lower body negative pressure (LBNP) insulin sensitivity reveals that, in normal subjects, a sudden increase in skeletal muscle noradrenergic activity antagonizes insulin-stimulated muscle glucose removal. Insulin resistance resulting from LBNP is due to metabolic effect of NE and beta-adrenoreceptors.

Objectives: This study aimed to indicate the feasibility of a prototype electrical neuromodulation system using a closed-loop energy-efficient ultrasound-based mechanism for communication, data transmission, and recharging., Materials and Methods: Closed-loop deep brain stimulation (DBS) prototypes were designed and fabricated with ultrasonic wideband (UsWB) communication technology and miniaturized custom electronics. Two devices were implanted short term in anesthetized Göttingen minipigs (N = 2). Targeting was performed using preoperative magnetic resonance imaging, and locations were confirmed postoperatively by computerized tomography. DBS systems were tested over a wide range of stimulation settings to mimic minimal, typical, and/or aggressive clinical settings, and evaluated for their ability to transmit data through scalp tissue and to recharge the DBS system using UsWB., Results: Stimulation, communication, reprogramming, and recharging protocols were successfully achieved in both subjects for amplitude (1V-6V), frequency (50-250 Hz), and pulse width (60-200 μs) settings and maintained for ≥six hours. The precision of pulse settings was verified with <5% error. Communication rates of 64 kbit/s with an error rate of 0.05% were shown, with no meaningful throughput degradation observed. Time to recharge to 80% capacity was <9 minutes. Two DBS systems also were implanted in the second test animal, and independent bilateral stimulation was successfully shown., Conclusions: The system performed at clinically relevant implant depths and settings. Independent bilateral stimulation for the duration of the study with a 4F energy storage and full rapid recharge were achieved. Continuous function extrapolates to six days of continuous stimulation in future design iterations implementing application specific integrated circuit level efficiency and 15F storage capacitance. UsWB increases energy efficiency, reducing storage requirements and thereby enabling device miniaturization. The device can enable intelligent closed-loop stimulation, remote system monitoring, and optimization and can serve as a power/data gateway to interconnect the intrabody network with the Internet of Medical Things., Competing Interests: Conflict of Interest Emrecan Demirors, Tommaso Melodia, and Jorge Jimenez are cofounders of Bionet Sonar Inc and hold equity interest. Raffaele Guida and Ryan Burke were employees of the company at the time of the study. Bionet Sonar holds all rights for the technology and its personnel, and its founders led the design, development, fabrication, and feasibility testing of prototype devices, including data collection and analysis, decision to publish, and preparation of this manuscript. Joseph S. Neimat serves as a consultant for Medtronic and on a scientific advisory board for Abbott. Steven C. Koenig reports one conflict of interest (spouse is paid by Bionet Sonar for her assistance with grants administration activities but did not participate in any research and development activities and/or participation in the preparation of the manuscript)., (Copyright © 2024 International Neuromodulation Society. Published by Elsevier Inc. All rights reserved.)

Besides acting complexly on both normal and tumor cells, transforming growth factor-beta (TGF-beta) can determine the nature of the response to the antigen, strongly inhibiting the differentiation of naive CD4+ T-cells toward a T helper-1 (Th-1) phenotype; in a number of experimental models, TGF-beta also appeared to be a potent immunosuppressant factor. TGF-beta was shown to be released by some human malignant mesothelioma (MMe) cells, which affects the immune response to this tumor. Thus, for a better understanding of the role of TGF-beta in the immune response to MMe cells, we evaluated the production of a Th-1 cytokine (IFN-gamma) and of a Th-2 cytokine (IL-4), following Purified Protein Derivative (PPD) recall antigen presentation by human MMe cells to a class-II major histocompatibility complex (MHC-II)-matched PPD clone (PPD clone). Our data confirm that human MMe cells possess the unusual capability of presenting a common recall antigen to CD4+ lymphocytes but also show that these tumor cells can abrogate Th-1 immune response, as evidenced by a shift in favor of the production of IL-4 over that of IFN-gamma, through a TGF-beta-mediated pathway; only the simultaneous block of TGF-beta1 and beta2 effects can significantly restore a typical Th-1 pattern of cytokine production by PPD clone in response to PPD presentation by MMe. Even though the role of TGF-beta in the promotion of MMe growth should be further and better defined, this effect should be considered when designing new therapeutical approaches aimed at improving the immune response to MMe.