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עמוד בית
Fri, 05.12.25

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February 2025
Shira Peretz PhD, Marina Kurtz MSc, Aviad Sivan PhD, Arnon Blum MD MSc

Background: Cardiovascular disease (CVD) events are rare in premenopausal women. Nevertheless, women with depression have a higher prevalence of CVD. Patients with depression present with endothelial dysfunction and impaired ability to regenerate endothelial progenitor cells (EPCs).

Objectives: To understand the association between depression and CVD, especially in young women.

Methods: We collected peripheral blood samples from 30 premenopausal women diagnosed with major depression and 28 aged-matched healthy women. From these blood samples, we extracted RNA and conducted RNA sequencing to obtain comprehensive gene expression profiles. Gene expression analysis was performed to identify differences between the two groups.

Results: We detected 6540 differentially expressed genes between the two groups, of which 5577 were downregulated and 963 up regulated. Of these genes, we detected a significant decrease of CD144 (VE-Cadherin) (P = 0.0001), CD146 (MCAM) (P = 0.0001) and CD133 (PROM1) (P = 0.00009), all known to enhance EPCs and regeneration of damaged blood vessels. A significant increase was found in the expression of CD31 (PECAM1) (P = 0.0003) and CD45 (PTPRC) (P = 0.00001), both known to promote atherogenesis and thrombogenesis with platelet and T lymphocyte activation.

Conclusions: Young premenopausal women with depression had an impaired ability to grow colony forming units of endothelial progenitor cells (CFU-EPCs). Young women with depression are more vulnerable genetically to develop CVD because of the downregulated genes of the stem cells endothelial vascular regeneration and upregulation of genes coding for platelet and T lymphocyte activation, thus accelerating the atherosclerotic and atherothrombotic pathway.

September 2010
H. Newman, S. Kurtz and R. David

Background: The existence of "ophthalmoltonic consensual reaction," a contralateral change in intraocular pressure in the fellow eye induced by treatment of the first eye only, was suggested in 1924. Since then, the validity of this mechanism has been controversial.

Objectives: To assess intraocular pressure changes in the contralateral fellow eyes of patients treated with IOP[1]-lowering medication in one eye, and investigate the existence of an ophthalmotonic consensual reaction.

Methods: The study population included 38 patients with newly diagnosed bilateral ocular hypertension or early open angle glaucoma. One eye of each patient was randomly treated with one of five compounds: prostaglandin analogues, beta-blockers, alpha-2 agonists, carbonic anhidrase inhibitors and a combination therapy: dorzolamide hydrochloride–timolol maleate (Cosopt®, Sharpe & Dohme). The eye with the higher baseline IOP was selected to be the treated eye. After 3 weeks a masked examiner measured the IOP in both the treated and untreated eye.

Results: Mean IOP of the treated eyes at baseline was 26.1 ± 4.2 mmHg and at follow-up 20.2 ±2.9 mmHg, a reduction of IOP from baseline of -6 ± 3.8 mmHg, a mean percent reduction of -22 ± 10.1%. In the contralateral eyes, the mean IOP at baseline was 24.2 ± 3 mmHg and 23.1 ± 3.1 mmHg at follow-up; IOP reduction from baseline was -1.2 ± 1.8 mmHg, or mean percent reduction -4.7 ± 7.1%. A major contralateral IOP decrease was seen only in the beta-blockers and the combination (Cosopt®) treatment groups (-6.1 ± 8.3% and -12.3 ± 8.3% mean percent reduction, respectively, P < 0.05). The contralateral eyes in the prostaglandin analogues, CAI[2] or α2-agonist groups showed only a small change in IOP (-2.6 ± 4.6%, -3.2 ± 2.6%, +0.7 ± 3.3%, mean percent reduction, respectively, P < 0.05).

Conclusions: The existence of an ophthalmoltonic consensual reaction was not supported.






[1] IOP = intraocular pressure



[2] CAI = carbonic anhidrase inhibitors


May 2010
A. Kesler, I. Haber and S. Kurtz

Background: Normal-tension glaucoma is a chronic progressive optic neuropathy of unknown etiology. Neuroimaging workup in these patients is controversial.

Objectives: To determine the value of routine neurologic and neuro-ophthalmologic evaluations in patients with NTG[1].

Methods: We conducted a retrospective review of all patients diagnosed with NTG in our institution between 2001 and 2006. Neurologic and neuro-ophthalmologic data were evaluated.

Results: Sixty-eight patients were considered suitable for the study (35 males, 33 females age range 43–90 years). Neurologic and neuro-ophthalmologic findings were normal in all of them. The computed tomography brain scan was normal in 88% and duplex carotid Doppler scan was normal in 92%.

Conclusions: Pathologic findings in neurologic and neuro-ophthalmologic assessments were uncommon in NTG. Therefore, contrary to earlier suggestions, neurologic and neuro-ophthalmologic evaluations in typical normal-tension glaucoma patients appear to have no added value.




 

[1] NTG  = normal-tension glaucoma


 

 
 
 
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