“I Did Not Have Sexual Relations with That Woman”

Teen vaping on a dark street.Recently, I sat across from an accomplished high school athlete who had just told me that he did not smoke and had not used any drugs. But when I asked directly about whether he vaped he openly said, “Of course!” He went on to explain that vaping isn’t smoking, isn’t unhealthy, and that THC is natural, not a drug.

Teen Vaping

By some reports, as many as 20 percent of high school students vape. And they often begin in middle school.

Juul is the top-selling e-cigarette brand (and very cuul among kids). A single Juul pod can contain as much nicotine as a pack of 20 regular cigarettes. Nicotine harms the developing adolescent brain. Moreover, e-cigarette aerosol is not harmless water vapor. It’s a chemical cocktail that’s inhaled deep into the delicate lungs. We don’t yet know the long-term effects.

The Tip of the Teen Vaping Iceberg

CDC is in the process of investigating multiple cases of severe pulmonary disease in people who use e-cigarettes. Some of the cases have been in people vaping THC; others in those who only vaped nicotine. Many have been hospitalized. Some have been placed on ventilators. The death toll is climbing.


Anyone who vapes who develops respiratory symptoms (cough, shortness of breath, chest pain) or GI symptoms (nausea, vomiting, diarrhea) should seek medical attention promptly.


 

The CDC has issued an official warning against using bootleg, street, or modified vaping products of any kind. They now advise that youth, young adults, and pregnant women should not use e-cigarettes of any kind.

The FTC, FDA, and several states attorneys general investigating Juul for the marketing conversations it may be having with our kids.

The Long Tail of Teen Vaping

Of the millions who vape, the numbers reported by the CDC are very small. But milder damage may be far more common than we yet realize. It’s not clear whether the damage is from contaminants or the vaped compounds themselves. These details are an important reminder that e-cigarettes are still new products whose health impacts are only beginning to be understood.

It’s time for us to have direct, respectful, and engaged conversations with our kids about vaping. Learn from them what they think and emphasize that they are the ultimate arbiters of what they put in their bodies. The CDC investigation is a great place to start the conversation.

The post “I Did Not Have Sexual Relations with That Woman” appeared first on DrGreene.com.

Aqeuous Lawsonia Inermis leaf extract alleviated aluminum-induced oxidative stress.

PMID: 

JBRA Assist Reprod. 2019 Apr 30 ;23(2):117-122. Epub 2019 Apr 30. PMID: 30875169

Abstract Title: 

Effects of Aqueous Leaf Extract of Lawsonia inermis on Aluminum-induced Oxidative Stress and Adult Wistar Rat Pituitary Gland Histology.

Abstract: 

OBJECTIVES: The aim of this study was to investigate the antioxidant effect of aqueous Lawsonia inermis leaf extract on aluminum-induced oxidative stress and the histology of the pituitary gland of adult Wistar rats.METHODS: Thirty-five adult male Wistar rats weighing between 100-196g and 15 mice of the same weight range were included in the study. Lawsonia inermis extracts and aluminum chloride (AlCl) were administered for a period of three weeks to five rats per group. The subjects in Group 1 (control) were given pellets and distilled water. Group 2 received 60mg/kg/d of aqueous extract of Lawsonia inermis. Group 3 was given 0.5mg/kg/d of AlCl. Group 4 was administered 0.5mg/kg/d of AlCland 60mg/kg/d of aqueous Lawsonia inermis extract orally. Group 5 received 0.5mg/kg/d of AlCland 75mg/kg/d of aqueous Lawsonia inermis extract orally. Group 6 was given 0.5mg/kg/d of AlCland 100mg/kg/d of aqueous Lawsonia inermis extract orally. Group 7 was administered 0.5mg/k/d of AlCland 5mg/Kg/d ascorbic acid in distilled water orally. Twenty-four hours after the last administration, the animals were weighed, sedated with chloroform, and had their pituitary glands located, removed, and weighed on an electronic analytical balance.RESULTS: Decreased cell counts were observed in the pituitary gland micrographs of the Wistar rats given 0.5mg of aluminum chloride, whereas the Wistar rats given 0.5mg of aluminum chloride and varying doses of Lawsonia inermis had increased dose-dependent cell counts.CONCLUSION: Aqeuous Lawsonia Inermis leaf extract increased the cell counts of the pituitary glands of adult male Wistar rats, in addition to alleviating aluminum-induced oxidative stress.

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The application of henna is recommended for healing grade one pressure ulcers.

PMID: 

Int J Prev Med. 2019 ;10:26. Epub 2019 Feb 15. PMID: 30967912

Abstract Title: 

The Effect of Henna () on Preventing the Development of Pressure Ulcer Grade One in Intensive Care Unit Patients.

Abstract: 

Background: Detecting pressure ulcer is an important nursing diagnostic and care requirement in patients hospitalized in Intensive Care Unit (ICU). The purpose of this study is to examine the effect of Lawsonia plant on pressure ulcer grade one in ICU patients.Methods: In this clinical trial, 72 patients eligible for hospitalization in hospitals of Isfahan University of Medical Sciences were divided randomly into two control and intervention groups. The standard program of skin care was implemented on both groups; in addition, a mixture of Lawsonia (henna) and distilled water was applied topically in the intervention group. The classification form of the International Pressure Ulcer Advisory Panel was used to identify grade one ulcers. Data were collected on the 1day through demographic information questionnaire and Braden pressure ulcer risk assessment scale. An infrared thermometer was used to record local temperature of the ulcers on a daily basis. Assessments were made based on Pressure Ulcer Scale for Healing (PUSH), and the pressure ulcer area was examined per square centimeter on the 1, 4, and 7days. The data were analyzed using SPSS 16.Results: The average change in the ulcer area per square centimeter in the control group increased by 29.9± 37.93 whereas it decreased by 3.54 ± 33.91 in the intervention group. The mean PUSH score decreased in the intervention group (5.36 ± 3.12) while it increased in the control group (1.91 ± 1.53). The average changes of PUSH score before and after the intervention showed a significant differencein both groups.Conclusions: With regard to the effect of henna on the reduction of ulcer area and the average PUSH score in ICU patients, the application of henna is recommended for healing grade one pressure ulcers.

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This study provides the preliminary clue that L. inermis may be a potential source of memory-enhancing and anti-oxidant compounds.

PMID: 

Medicina (Kaunas). 2019 May 22 ;55(5). Epub 2019 May 22. PMID: 31121979

Abstract Title: 

Markedly Improves Cognitive Functions in Animal Models and Modulate Oxidative Stress Markers in the Brain.

Abstract: 

Medicinal plants represent an important source of alternative medicine for the management of various diseases. The present study was undertaken to assess the potential ofethanol (Li.Et) and chloroform (Li.Chf) extracts as memory-enhancing agents in experimental animals.Li.Et and Li.Chf were phytochemically characterized via gas chromatography-mass spectroscopy (GC-MS). Samples were tested for nootropic potentials at doses of 25, 50, 100, 200 mg/kg (per oral in experimental animals (p.o.)). Swiss albino mice of either sex (= 210) were divided into 21× 10 groups for each animal model. Memory-enhancing potentials of the samples were assessed using two methods including"without inducing amnesia"and"induction of amnesia"by administration of diazepam (1 mg/kg, intraperitoneally. Piracetam at 400 mg/kg (i.p.) was used as positive control. Cognitive behavioral models including elevated plus maze (EPM) and the passive shock avoidance (PSA) paradigm were used. Biochemical markers of oxidative stress such as glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) levels were analyzed in the brain tissue of treated mice.In 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals scavenging assay, Li.Et and Li.Chf exhibited 70.98± 1.56 and 66.99 ± 1.76% inhibitions respectively at 1.28 mg/mL concentration. GCMS results revealed the presence of important phytochemicals. Both samples (Li.Et and Li.Chf) at 25 mg/kg (p.o.) dose significantly (

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Wound healing effect of Lawsonia inermis.

PMID: 

Skin Pharmacol Physiol. 2019 Aug 29:1-12. Epub 2019 Aug 29. PMID: 31466077

Abstract Title: 

Wound Healing Effect of Lawsonia inermis.

Abstract: 

BACKGROUND: Lawsonia inermis-extracted oil is known for therapeutic properties, especially wound healing. This study assesses the potential of this oil for wound healing in a rat model.METHODOLOGY: To assess the potential of L. inermis-extracted oil for wound healing, phytochemical, antibacterial, and antioxidant analyses were conducted. Uniform wound excision was induced on the dorsum of randomly selected rats divided into 3 groups cleaned and treated with saline solution (control), Cicaflora (reference), and L. inermisoil. Biopsies performed after healing were histologically assessed.CONCLUSIONS: The quality and content of the fatty acids in the oil were determined. Results showed a high content of bioactive components inducing an efficient wound healing effect determined by an in vivo study. Histological and chromatic assessment findings revealed healing in the oil-treated group but not in the untreated group, a full reepithelialization with reappearance of skin appendages and well-organized collagen fibers without any inflammatory cells. This might be due to a synergistic effect of the phytoconstituents present in the oil.

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Honokiol can effectively activate cholangiocarcinoma apoptosis and increase the release of damage-associated molecular patterns.

PMID: 

World J Gastroenterol. 2019 Aug 7 ;25(29):3941-3955. PMID: 31413529

Abstract Title: 

Honokiol-enhanced cytotoxic T lymphocyte activity against cholangiocarcinoma cells mediated by dendritic cells pulsed with damage-associated molecular patterns.

Abstract: 

BACKGROUND: Cholangiocarcinoma or biliary tract cancer has a high mortality rate resulting from late presentation and ineffective treatment strategy. Since immunotherapy by dendritic cells (DC) may be beneficial for cholangiocarcinoma treatment but their efficacy against cholangiocarcinoma was low. We suggest how such anti-tumor activity can be increased using cell lysates derived from an honokiol-treated cholangiocarcinoma cell line (KKU-213L5).AIM: To increase antitumour activity of DCs pulsed with cell lysates derived from honokiol-treated cholangiocarcinoma cell line (KKU-213L5).METHODS: The effect of honokiol, a phenolic compound isolated from, on choangiocarcinoma cells was investigated in terms of the cytotoxicity and the expression of damage-associated molecular patterns (DAMPs). DCs were loaded with tumour cell lysates derived from honokiol-treated cholangiocarcinoma cells their efficacy including induction of T lymphocyte proliferation, proinflammatory cytokine production and cytotoxicity effect on target cholangiocarcinoma cells were evaluated.RESULTS: Honokiol can effectively activate cholangiocarcinoma apoptosis and increase the release of damage-associated molecular patterns. DCs loaded with cell lysates derived from honokiol-treated tumour cells enhanced priming and stimulated T lymphocyte proliferation and type I cytokine production. T lymphocytes stimulated with DCs pulsed with cell lysates of honokiol-treated tumour cells significantly increased specific killing of human cholangiocarcinoma cells compared to those associated with DCs pulsed with cell lysates of untreated cholangiocarcinoma cells.CONCLUSION: The present findings suggested that honokiol was able to enhance the immunogenicity of cholangiocarcinoma cells associated with increased effectiveness of DC-based vaccine formulation. Treatment of tumour cells with honokiol offers a promising approach as anDC-based anticancer vaccine.

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Nanoparticulated honokiol mitigates cisplatin-induced chronic kidney injury.

PMID: 

Antioxidants (Basel). 2019 Oct 9 ;8(10). Epub 2019 Oct 9. PMID: 31600935

Abstract Title: 

Nanoparticulated Honokiol Mitigates Cisplatin-Induced Chronic Kidney Injury by Maintaining Mitochondria Antioxidant Capacity and Reducing Caspase 3-Associated Cellular Apoptosis.

Abstract: 

Cisplatin is a potent anti-cancer drug, however, its accompanied organ-toxicity hampers its clinical applications. Cisplatin-associated kidney injury is known to result from its accumulation in the renal tubule with excessive generation of reactive oxygen species. In this study, we encapsulated honokiol, a natural lipophilic polyphenol constituent extracted frominto nano-sized liposomes (nanosome honokiol) and examined the in vivo countering effects on cisplatin-induced renal injury. We observed that 5 mg/kg body weight. nanosome honokiol was the lowest effective dosage to efficiently restore renal functions of cisplatin-treated animals. The improvement is likely due the maintenance of cellular localization of cytochrome c and thus preserves mitochondria integrity and their redox activity, which as a consequence, reduced cellular oxidative stress and caspase 3-associated apoptosis. These improvements at the cellular level are later reflected on the observed reduction of kidney inflammation and fibrosis. In agreement with our earlier in vitro study showing protective effects of honokiol on kidney cell lines, we demonstrated further in the current study, that nanosuspension-formulated honokiol provides protective effects against cisplatin-induced chronic kidney damages in vivo. Our findings not only benefit cisplatin-receiving patients with reduced renal side effects, but also provide potential alternative and synergic solutions to improve clinical safety and efficacy of cisplatin treatment on cancer patients.

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Investigation of anti-inflammatory and analgesic activities of camel milk in animal models.

PMID: 

Pak J Pharm Sci. 2019 Jul ;32(4(Supplementary)):1879-1883. PMID: 31680087

Abstract Title: 

Investigation of anti-inflammatory and analgesic activities of camel milk in animal models.

Abstract: 

Opioids and non-opioids have long been used as analgesic, anti-inflammatory and antipyretic. Long-term use of these drugs may lead to severe toxicities. Therefore natural remedies are now being explored to avoid risk of adverse effects associated with the use of these conventional medicines. Bioactive components from milk of different species have been identified as nutraceuticals, but no experimental or clinical study is conducted so far to explore the analgesic and anti-inflammatory potential of camel milk. In this study we evaluated camel milk for its possible analgesic and antiinflammatory activity. The anti-inflammatory effects of camel milk was studied in rats using paw edema method (induced by acetic acid) while tail-flick method was used to evaluate its analgesic effect in mice. Significantly increased tail-flick latency was shown after camel milk (33ml/kg) treatment when compared with acetylsalicylic acid at all time intervals. Anti-inflammatory activity of camel milk was significant (p

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Exploring the active mechanism of berberine against liver cancer by systematic pharmacology and experimental validation.

PMID: 

Mol Med Rep. 2019 Nov ;20(5):4654-4664. Epub 2019 Sep 23. PMID: 31545468

Abstract Title: 

Exploring the active mechanism of berberine against HCC by systematic pharmacology and experimental validation.

Abstract: 

Berberine (BBR) is the main component of Coptidis rhizoma, the dried rhizome of Coptis chinensis and is a potential plant alkaloid used for the treatment of cancer due to its high antitumor activity. The present study examined the therapeutic potential and molecular mechanism of action of BBR against HCC, using systematic pharmacology combined with a molecular docking approach and experimental validation in vitro. Through systematic pharmacological analysis, it was found that BBR serves a significant role in inhibiting HCC by affecting multiple pathways, especially the PI3K/AKT signaling pathway. Furthermore, the docking approach indicated that the binding of BBR to AKT couldlead to the suppression of AKT activity. The present study examined the inhibitory effect of BBR on the PI3K/AKT pathway in HCC and identified that BBR downregulated the expressions of phosphorylated AKT and PI3K in MHCC97‑H and HepG2 cells, inhibiting their growth, cell migration and invasion ina dose‑dependent manner. In addition, inhibition of the AKT pathway by BBR also contributed to cell apoptosis in MHCC97‑H and HepG2 cells. Taken together, the results of the present study suggested that BBR may be a promising antitumor drug for HCC that acts by inhibiting the PI3K/AKT pathway.

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Berberine protected C17.2 NSCs from oxidative damage then induced them to differentiate into neurons.

PMID: 

Front Cell Neurosci. 2019 ;13:395. Epub 2019 Sep 3. PMID: 31551713

Abstract Title: 

Berberine Protects C17.2 Neural Stem Cells From Oxidative Damage Followed by Inducing Neuronal Differentiation.

Abstract: 

Neurodegeneration is the loss of structure and/or function of neurons. Oxidative stress has been suggested as one of the common etiology in most of the neurodegenerative diseases. Previous studies have demonstrated the beneficial effects of berberine in various neurodegenerative and neuropsychiatric disorders. In this study, we hypothesized that berberine could protect C17.2 neural stem cells (NSCs) from 2,2'-Azobis(2-amidinopropane) dihydrochloride (AAPH)-induced oxidative damage then promote neuronal differentiation. AAPH was used to induce oxidative damage. After the damage, berberine protected C17.2 cells were kept cultured for another week in differentiation medium with/without berberine. Changes in cell morphology were detected by microscopy and cell viability was determined by MTT assay. Real-time PCR and western blot analysis were performed to confirm the associated pathways. Berberine was able to protect C17.2 NSCs from the oxidative damage. It lowered the cellular reactive oxygen species (ROS) level in C17.2 cells via Nuclear Factor Erythroid 2-Related Factor 1/2 (NRF1/2) – NAD(P)H Quinone Dehydrogenase 1 (NQO-1) – Heme Oxygenase 1 (HO-1) pathway. It also down-regulated the apoptotic factors-Caspase 3 and Bcl2 Associated X (Bax) and upregulated the anti-apoptotic factor-Bcl2 to reduce cell apoptosis. Besides, berberine increased C17.2 cell viability via up-regulating Extracellular-signal-Related Kinase (ERK) and phosphor-Extracellular-signal-Related Kinase (pERK) expression. Then, berberine promoted C17.2 cell to differentiate into neurons and the differentiation mechanism involved the activation of WNT/β-catenin pathway as well as the upregulation of expression levels of pro-neural factors Achaete-Scute Complex-Like 1 (ASCL1), Neurogenin 1 (NeuroG1), Neuronal Differentiation 2 (NeuroD2) and Doublecortin (DCX). In conclusion, berberine protected C17.2 NSCs from oxidative damage then induced them to differentiate into neurons.

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