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ificant withdrawal symptoms. Knowledge of this newly reported adverse manifestation can aid physicians in the diagnosis of gabapentin toxicity and prompt treatment, as gabapentin levels are not widely or immediately available.

Pathologic laughing, characterized by episodes of abrupt and inappropriate laughter occurring irrespective of a person's emotional feelings, has been reported in patients with neurologic deficits. Some pharmacotherapies, including selective serotonin reuptake inhibitors, are effective in alleviating pathologic laughing. However, contrary to previous reports, we report a case of pathologic laughing that developed after a patient with pontine hemorrhage was administered atomoxetine (Strattera).

A 55-year-old man was diagnosed with acute intracerebral hemorrhage in the right pons and midbrain. The patient showed mild cognitive impairment, and he was administered 10 mg of atomoxetine once daily as a cognitive enhancer. On the day of atomoxetine administration, he suddenly developed episodes of inappropriate laughter that was uncontrollable. The Pathological Laughter and Crying Scale showed a score of 4 of 54 on the day he started taking atomoxetine, and his score was 18 on the second day. He was administered atomoxetine for 3 consecutive days, but it was stopped on the fourth day. His laughing diminished, and his score improved to 5. His smiling expression and a score of 1 on the scale lasted for 1 week. On day 8 of drug discontinuation, his score was zero and all symptoms disappeared.

Previously, no single medication has been reported to cause pathologic laughing. Atomoxetine is a stimulant that increases norepinephrine and dopamine levels in the prefrontal cortex. This report suggests that, unlike what is known thus far, norepinephrine and dopamine might play a crucial role in the development of pathologic laughing.

Previously, no single medication has been reported to cause pathologic laughing. Atomoxetine is a stimulant that increases norepinephrine and dopamine levels in the prefrontal cortex. This report suggests that, unlike what is known thus far, norepinephrine and dopamine might play a crucial role in the development of pathologic laughing.

Breast cancer (BC) is a common malignancy with highly female incidence. So far the function of notoginsenoside R1 (NGR1), the extract from Panax notoginseng, has not been clearly elucidated in BC.

Optimal culture concentration and time of NGR1 were investigated by cell counting kit-8 assay. Cell proliferation ability was measured by colony formation assays. Transwell assay was used to detect the effect of NGR1 on cell migration and invasion. The apoptosis rate of cells between each group was measured by TUNEL assay.

NGR1 treatment has an inhibitory effect on proliferation, migration, invasion, and angiogenesis and a stimulating effect on cell cycle arrest and apoptosis of Michigan Cancer Foundation-7 (MCF-7) cells. The 50% growth inhibitory concentration for MCF-7 cells at 24 h was 148.9 mmol/L. bpV chemical structure The proportions of MCF-7 cells arrested in the G0/G1 phase were 36.94±6.78%, 45.06±5.60%, and 59.46±5.60% in the control group, 75, and 150 mmol/L groups, respectively. Furthermore, we revealed that NGR1 treatment attenuates BC progression by targeted downregulating CCND2 and YBX3 genes. Additionally, YBX3 activates phosphatidylinositol 3-phosphate kinase (PI3K)/protein kinase B (Akt) signaling pathway by activating kirsten rat sarcoma viral oncogene, which is an activator of the PI3K/Akt signaling pathway.

These results suggest that NGR1 can act as an efficacious drug candidate that targets the YBX3/PI3K/Akt axis in patients with BC.

These results suggest that NGR1 can act as an efficacious drug candidate that targets the YBX3/PI3K/Akt axis in patients with BC.

To examine 5-year survival in esophageal cancer after minimally invasive esophagectomy (MIE) compared to open esophagectomy (OE).

MIE is becoming an increasingly common approach in the surgical treatment of esophageal cancer. A recent meta-analysis suggested 18% lower 5-year all-cause mortality after MIE compared to OE, but the quality of the included studies was limited.

Population-based cohort study including almost all patients who underwent elective esophagectomy for esophageal cancer in Sweden or Finland in 2010-2016, with follow-up until 2020. Cox regression was used to provide hazard ratios (HRs) with 95% confidence intervals (CIs) of all-cause 5-year mortality (main outcome) after MIE (hybrid or total) versus OE. Adjustments were made for age, sex, comorbidity, pathological tumor stage, histological tumor type, neoadjuvant chemo(radio)therapy, country, and annual hospital volume of esophagectomy.

Among all 1,264 patients, 470 (37.2%) underwent MIE and 794 (62.8%) underwent OE. MIE was associated with an 18% decreased risk of all-cause 5-year mortality, compared to OE (adjusted HR 0.82, 95% CI 0.67-1.00 [P = 0.048]). The HR of all-cause 5-year mortality was seemingly lower after total MIE compared to OE (adjusted HR 0.77, 95% CI 0.60-0.98) than after hybrid MIE compared to OE (adjusted HR 0.87, 95% CI 0.68-1.11).

This bi-national study indicates that MIE is associated with a higher 5-year survival than OE in patients with esophageal cancer, and that the survival benefit is greater after total MIE than hybrid MIE.

This bi-national study indicates that MIE is associated with a higher 5-year survival than OE in patients with esophageal cancer, and that the survival benefit is greater after total MIE than hybrid MIE.

The Lothian Birth Cohort 1936 (LBC1936) is a highly phenotyped longitudinal study of cognitive and brain ageing. Given its substantial clinical importance, we derived an indicator of mild cognitive impairment (MCI) and amnestic and nonamnestic subtypes at 3 time points.

MCI status was derived at 3 waves of the LBC1936 at ages 76 (n=567), 79 (n=441), and 82 years (n=341). A general MCI category was derived as well as amnestic MCI (aMCI) and nonamnestic MCI (naMCI). A comparison was made between MCI derivations using normative data from the LBC1936 cohort versus the general UK population.

MCI rates showed a proportional increase at each wave between 76 and 82 years from 15% to 18%. Rates of MCI subtypes also showed a proportional increase over time aMCI 4% to 6%; naMCI 12% to 16%. Higher rates of MCI were found when using the LBC1936 normative data to derive MCI classification rather than UK-wide norms.

We found that MCI and aMCI rates in the LBC1936 were consistent with previous research. However, naMCI rates were higher than expected.